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Overview of gut flora and probiotics pdf 2014,compound digestive enzyme capsules,probiotic nu skin postavy - Easy Way

You must have JavaScript enabled in your browser to utilize the functionality of this website. Colonix Program is a comprehensive 30-day, three-part cleansing system that includes: Paranil®, Colonix® daily fiber and KleriTea® herbal tea. Flora Protect® is an all natural, vegetarian probiotic supplement packed with eight beneficial bacteria species to maintain a beautifully balanced intestinal flora. As part of the Toxinout Program, Flora Protect Probiotics support a healthy system as they replenish beneficial bacteria to the GI tract. Most detox programs fail to address the fact that the modern diet (sugar, caffeine, white bread) and the use of antibiotics may result in reduction of good bacteria in the GI tract. If you are considering a first-time cleanse, we recommend you commit to a full 90-day cleanse with the Colonix Program, adding Toxinout Program (which contains a 30-day supply of Flora Protect) in the second month. A probiotic supplement should also contain FOS, or prebiotics, which is food that helps the bacteria survive its long journey to your intestines.
As a global leader in cleansing and detoxification, DrNatura voluntarily adheres to the FDA’s strictest quality standards for dietary supplements via current Good Manufacturing Practices. When possible, DrNatura uses all natural ingredients that are processed minimally for optimal nutrition. WARNING: DrNatura® products should not be used by pregnant or nursing women, by children (except children’s products), or by anyone with a serious medical condition. KleriTea® herbal tea contains senna and is designed for short-term and occasional use only. Science, Technology and Medicine open access publisher.Publish, read and share novel research.
Variations on the Efficacy of Probiotics in PoultryLuciana Kazue Otutumi1, Marcelo Biondaro Gois1, Elis Regina de Moraes Garcia2 and Maria Marta Loddi3[1] Universidade Paranaense,, Brazil[2] Universidade Estadual do Mato Grosso do Sul,, Brazil[3] Universidade Estadual de Ponta Grossa,, Brazil1.
From there, several studies have been made and continue being developed with the use of probiotics.
Probiotics Applications in Autoimmune DiseasesHani Al-Salami 1, Rima Caccetta1, Svetlana Golocorbin-Kon 2 and Momir Mikov2[1] School of Pharmacy, Curtin Health Innovation Research Institute, Curtin University of Technology, Perth WA, Australia[2] Pharmacy Faculty, University of Montenegro, Podgorica, Montenegro1.
Product: Khush balanced flora probiotic supplement aids in maintaining a healthy balance of intestinal flora.
We promise to never spam you, and just use your email address to identify you as a valid customer. The Balancing Flora Probiotic Supplement is the only product that has worked for me to help manage my system. Have been taking this product for 2 months and have not had any issues with yeast or urinary tract infections. After being on many medications for autoimmune issues and suffering from the side effects, my doctor recommended that I try the Khush probiotic to see if it would help. This is a great product to use if you're prone to yeast infections after being prescribed antibiotics. International Shipping - items may be subject to customs processing depending on the item's declared value. Your country's customs office can offer more details, or visit eBay's page on international trade. Estimated delivery dates - opens in a new window or tab include seller's handling time, origin ZIP Code, destination ZIP Code and time of acceptance and will depend on shipping service selected and receipt of cleared payment - opens in a new window or tab.
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Will usually ship within 1 business day of receiving cleared payment - opens in a new window or tab. By submitting your bid, you are committing to buy this item from the seller if you are the winning bidder. By clicking Confirm, you commit to buy this item from the seller if you are the winning bidder. By clicking Confirm, you are committing to buy this item from the seller if you are the winning bidder and have read and agree to the Global Shipping Program terms and conditions - opens in a new window or tab. Your bid is the same as or more than the Buy It Now price.You can save time and money by buying it now. Definition: Live microorganisms which, when administered in adequate amounts, confer a health benefits on the host.
Probiotics or known as good bacteria, are friendly and beneficial microorganism that lived in your gut flora. Definition: Nondigestible substances that provide a beneficial physiological effect for the host by selectively stimulating the favourable growth or activity of a limited number of indigenous bacteria.
Prebiotics are dietary substances (mostly consisting of nonstarch substances poorly digested by human enzymes) that nurture a selected group of microorganisms living in the gut. Prebiotics – Food (nourish and sustain) for probiotics, stimulating the growth of friendly bacteria which in turn maintain a healthy digestive environment. Promotes a regular and healthy digestive system by replenishing your intestinal flora with proven strains of human-source bacteria.
Stress, poor nutrition, prescription drugs, alcohol, and caffeine all compromise this colony, and your health. Probiotics are key to maintaining a regular digestive tract that consistently removes waste and toxins. Probiotics are your first line of defense and are critical for a normal immune response to harmful invaders. Probiotics make vitamins, extract nutrients from food and ensure proper absorption of nutrients. NOTE: Pregnant or lactating women, diabetics, children under age 12, hypoglycemics, and people with known medical conditions should consult with a physician prior to taking supplements. Studies have uncovered the fact that most probiotics on the market have a very high percentage of dead organisms, making them useless. Vegetable (palm) oil, gelatin (fish source), glycerin, lecithin, pectin and caramel coloring. You can’t evict them, but you can help keep the bad bacteria in check by populating your gut with beneficial strains, like Lactobacilli, Bifidobacteria and Streptococcus.
You need beneficial bacteria in your gut to help balance your intestinal flora, which can become unbalanced with "bad" bacteria.
Flora Protect Probiotics contains no artificial colors or flavors, no yeast, no starch, no wheat or gluten , no salt, no milk, no egg and no shellfish. We guarantee your complete satisfaction with each and every DrNatura product by offering a 60-day, no-questions-asked money-back policy. Do not use this product if you are allergic to soy or have a medical condition that can be affected by consumption of soy. Proposed interactions between competitive exclusion products, probiotics or immunostimulants, and avian intestinal immunity. IntroductionIn face of the current debate about the use of antibiotics as growth promoters, due to the probable relationship with resistance to antibiotics used in human medicine, the presence of antibiotic residues in products of animal origin intended for human consumption and the emergent demand from consumer market for products free from additive residues, it was necessary to search for alternative products that could replace antibiotics used as promoters, without causing losses to productivity or product quality. Inconsistent results from the use of probiotics in animal production have been a constraint for the promotion of their use. Molecular mimicry as a proposed cause of autoimmune diseases through the induction of ‘mistaken-identity’ immune response.5. The relationship between LPS endotoxins and inflammation pathology in some autoimmune diseases. IntroductionAn autoimmune disorder (AD) is a condition in which the immune system mistakenly attacks its own body cells through the production of antibodies that target certain tissues.
I haven't had any of the IBS symptoms that I have been experiencing the past few years! Contact the seller- opens in a new window or tab and request a shipping method to your location.
You have read and agree to the Global Shipping Program terms and conditions - opens in a new window or tab. Import charges previously quoted are subject to change if you increase you maximum bid amount. They are live microbes that can be formulated into many different types of products, including foods such as yoghurt and other dairy products, drugs, and dietary supplements. They enhance the immune system by favorably altering the gut micro-ecology and preventing unfriendly organisms from gaining a foothold in the body. It’s where harmful invaders are disarmed, energy is extracted from food, and toxins are removed. QORE Probiotics give you billions of new, fresh, healthy bacteria, delivered right to your gut.
Fragile probiotics that require refrigeration make it even more difficult to thrive from the factory to your gut.
Flora Protect capsules are coated with a special protective layer to ensure that the bacteria survive all the way to the colon. If you are taking any medications, consult with a healthcare professional before using DrNatura products. Schematic representation of the crosstalk between probiotic bacteria and the intestinal mucosa.
Effectiveness of probiotics in the prevention of Salmonella colonization in broiler chicken.
An alternative is the use of probiotics, which are products made from living micro-organisms or their L-forms (without cell wall). Variations in the efficacy of probiotics can be due to the difference in microbial species or micro-organism strains used, or with the additive preparation methods (Jin et al., 1998a). Such attack triggers further inflammation that result in more attacks and a significant inflammatory response leading to tissue destruction and cessation of functionality [1]. Healthy intake of probiotics is integral to nurturing optimal genital and bladder function. If you reside in an EU member state besides UK, import VAT on this purchase is not recoverable.
They prevent the overgrowth of yeast and fungus and produce substances that can lower cholesterol.When the ratio of good bacteria to bad is lowered, problems begin to arise such as excessive gas, bloating, constipation, intestinal toxicity and poor absorption of nutrients. These important duties are performed by probiotics – the trillions of friendly bacteria that live in your intestines.
Our world-class delivery system is superior to any other method for keeping the bacteria alive until they reach your intestine where they can thrive and multiply.
Many companies ignore the fact that probiotics die in stomach acid and offer liquid, capsule, or food-infused probiotics that have a low probability of making it into the gut alive. Customers whose testimonials are published on the web site receive a free canister of Colonix® fiber (a $35.00 value).
The micro-organisms included as probiotics are usually assumed to be non-pathogenic components of the normal microflora, such as the lactic acid bacteria. However, other factors can justify the variations in the results of probiotic use in poultry, such as origin species, probiotic preparation method, survival of colonizing micro-organisms to the gastrointestinal tract conditions, environment where the birds are raised, management (including the application time and application route of the probiotic), the immunologic status of the animals, the lineage of the poultry evaluated, as well as age and concomitant use or not of antibiotics. ADs include diabetes, rheumatoid arthritis, Graves' disease, systemic lupus and inflammatory bowel disease (IBD) [2]. A good probiotic supplement will contain millions and millions of live bacteria to bolster and replenish levels of health promoting good bugs in your digestive tract. Qore Probiotic is delivered in the protective Trisphere® capsule, ensuring the probiotics are properly shielded from temperature fluctuations, external environment, and stomach acid.
Probiotic bacteria can also enhance intestinal barrier function by (5) increasing mucus production (Adapted Ng et al., 2009).
However, there is good evidence that non-pathogenic variants of pathogenic species can operate in much the same way as traditional probiotics. Thus, the aim of this review is to discuss the use of probiotics in poultry, with emphasis on the type of probiotic and micro-organisms used, action mechanism and its relation with the variations on the results of poultry survey.2.
ADs are on the rise worldwide and have major health implications from the diseases themselves as well as complications. Once there, these probiotic reinforcements join forces with the existing friendly bacteria to help inhibit the growth of more harmful microbes. Laboratory results demonstrate Qore is up to twice as effective for keeping probiotics alive and healthy until they’re delivered to their new home in your intestine. For example, avirulent mutants of Escherichia coli, Clostridium difficile, and Salmonella Typhimurium can also protect against infection by the respective virulent parent strain (Fuller, 1995). Type of probiotic and micro-organisms usedThere are several types of probiotics available in the market to be used in poultry, with a range of micro-organisms present and, therefore, with different metabolic activities and action modes. Even though the causes of AD have been postulated to be genetic and environmental, the actual triggers remain poorly defined [3]. Also, they present variations as to the capacity of colonizing the intestine or not, which justifies variations on the results of their use.Bacillus, Bifidobacterium, Enterococcus, E.
In their experiments, the authors observed that the intestinal contents of normal adult birds, orally administered to chicks with one day of age, altered their sensitivity to infection by Salmonella spp. Previous figures underestimated the scope of the problem, while even the most pessimistic predictions fell short of the current figure. However, even those belonging to the same species can have different strains and even these different strains from the same species can have different metabolic activities.
It is predicted that the total number of people living with AD will increase drastically within the coming thirty years if no new and substantially more effective drugs are produced [4].
On 2009, estimated health costs of autoimmune disorders have exceeded 100 billion dollars only in the US. This adds to the cost generated from higher rate of hospitalization, higher mortality rate, and impaired performance of workers with the disease [5].
AD is a condition that incorporates various metabolic disturbances and inflammatory physiological and biochemical reactions including blood dyscrasias and endocronological and pathophysiological imbalances.
Of recently, gastrointestinal abnormalities have been directly linked to the initiation and progression of autoimmune diseases especially slower gut movement (gastroparesis) and microfloral overgrowth (especially of fermentation bacteria and yeasts due to the slightly more acidic gut contents). This product is dairy-free and does not contain artificial colours, flavours or sweeteners, preservatives, chemical additives, wheat, yeast or animal derivatives.
Improving AD complications, reducing prevalence and restoring normal physiological patterns should significantly optimise treatment outcomes and the quality of life for patients.In healthy individuals, the immune system prevents self-attack by two main routes. Firstly, by neutralizing dysfunctional lymphocytes in the thymus before they start attacking own body cells.
This results in preventing the initiation of inflammation and progression of the autoimmune symptoms. Secondly, when dysfunctional lymphocytes are released into the mainstream, the immune system minimizes their ability to interact with triggers (antigens) through direct and indirect effects [6-8]. This results in a significant reduction in the severity of potential inflammatory response.
Accordingly, treating AD can be achieved by either replacing the function of the damaged tissues (e.g. Generally, clinical and laboratory research has suggested that certain immune cells called B-cells may have a stronger influence on the development and progression of various autoimmune diseases than previously thought [12]. In T1D, the autoimmune system attacks the ?-cells of the pancreas triggering an inflammatory reaction, which results in the destruction of these cells and the cessation of insulin production [13]. In rheumatoid arthritis, rheumatoid factor antibodies are produced by the immune system and are interact with ? globulin (blood proteins) forming a complex that triggers inflammation that targets muscles and bones [14]. In Graves’s diseases, an autoimmune disease of the thyroid gland, antibodies are produced against the thyroid protein thyroglobulin.
These antibodies are called Thyroid Stimulating Hormones Receptors (TSHR) antibodies results in the increase in thyroid synthesis and section and thyroid growth as well as all accompanying symptoms [15-17]. In some autoimmune blood disorders, antibodies are produced against the body red and white blood cells, while in other autoimmune disorders, antibodies attack a wide range of tissues and organs resulting in more debilitating symptoms [18]. In systemic lupus, antibodies target antigens that are present in nucleic acids and cell organelles such as ribosomes and mitochondria. The inflammation in both conditions can affect the small and large intestine and sometimes other parts of the digestive system.
Generally, ulcerative colitis is limited to the colon, primarily affecting the mucosa and the lining of the colon. Extensive inflammation gives rise to small ulcerations and microscopic abscesses that produce bleeding which exacerbate further the inflammatory response and worsen symptoms. Crohn's disease affects the small and large intestine, and rarely the stomach or oesophagus. Many ADs have been characterized by a compromised gut movement which has been linked to the disturbed immune system and can result in substantial gut bacterial and yeast overgrowth [20-24].
Such an overgrowth is postulated to disturb body physiological and biochemical reactions and exacerbate the autoimmune-associated inflammation.
This has also been linked to long term complications and weaker prognosis resulting in poor drug response and worsening quality of life [25, 26]. Diagnosing autoimmune diseases can be particularly difficult, because these disorders can affect any organ or tissue in the body and produce a wide variety of signs and symptoms. Many early symptoms of these disorders — such as fatigue, joint and muscle pain, fever or weight change — are nonspecific.
Accordingly, prevention in most susceptible individuals and early diagnosis are two most important approaches, when researching the future therapy for autoimmune diseases.ADs include wide range of inflammatory disease models that are characterized by the presence of a colossal inflammatory response.
The trigger of the inflammation is versatile and complex with many hypotheses ranging from ingested toxins to idiopathic causes [9, 18, 27]. However, genetic influence remains a strong cause and is considered a contributing factor for the development and progression of these diseases.
AD-associated inflammation can cause chemical unbalance that has been linked to poor tissue sensitivity to drug stimulation, rise in the levels of reactive radicals in the blood, poor enterohepatic recirculation and negatively affecting liver detoxification and performance. The level and extent of tissue damage depend on the severity of the inflammatory response and varies in different disease models.
Accordingly, future therapy should focus not only on symptomatic relief, but also on rectifying the disturbances in body physiology and associated short and long term complications.
These disturbances may affect the whole body and have been strongly linked to inflammatory lymph nodes in the gut walls.
Thus, future therapy should also focus on normalizing gut disturbed immune response, which can be achieved through normalizing the composition of bile acids and microflora, gut immune-response and microflora-epithelial interactions towards maintaining normal biochemical reactions and healthy body physiology.


Of recently, the applications of probiotics in autoimmune diseases have gained great interest due to the feasibility of their administration and also their safety. A good example is hypoglycemic effect of probiotics in a rat model of Type 1 diabetes [28]. Possible mechanisms of actions include their anti-inflammatory effect resulting in a significant reduction in diabetes progression and complications [24]. This can be brought about through the normalization of gut disturbed-microflora by the administered probiotic-bacteria. Interesting, probiotic co-administration with a sulphonylureas antidiabetic drug has shown to reduce inflammation and ameliorate diabetes complications suggesting a significant role and great potential of probiotic applications as anti-inflammatory adjunct therapy. Probiotics are dietary supplements containing bacteria which, when administered in adequate amounts, confer a health benefit on the host. Combinations of different bacterial strains can be used but a mixture of Lactobacilli and Bifidobacteria is a common choice.
Probiotics have been shown to be beneficial in a wide range of conditions including infections, allergies, metabolic disorders such as diabetes mellitus, ulcerative colitis and Crohn’s disease.This chapter aims to explore the changes in gut microflora, physiology and metabolic pathways which are associated with the autoimmune diseases.
A great focus will be on the potential application of probiotics on rectifying the disturbed gut composition associated with these diseases and whether such intervention can prevent or even treat these diseases. Autoimmune-associated disturbances in gut microfloraThe initial set of gut microfloral composition in human starts during birth.
The physical structure of the gut is altered by the presence of microorganisms during growth. Once matured, the integrity of the epithelial barrier is maintained by the presence of these same microbes. Accordingly, the mother’s microflora is considered a source of the infant own initial gut bacterial colonization, which is then influenced by the mother’s milk, tissues’ growth, the maturation of the immune system, as well as other factors.
Gut motility and contents have been emerging as an important area of research when investigating the origin and potential therapeutics of autoimmune disease. Many patients with autoimmune disease have shown strong evidence of disturbances in the composition of gut microflora and the subsequent toxin buildup and other associated physiological and biochemical abnormalities [29]. Although the pathogenesis of T1D remains unclear, there is strong evidence supporting the hypothesis that the trigger leading to T1D, starts in the gut of genetically susceptible individuals [30, 31].
This inflammation causes major disturbances in both, the gut microfloral composition and bile acids ratios.
This results in ongoing inflammatory response that brings about the destruction of pancreatic tissues and subsequent cessation of insulin production leading to clinical signs and symptoms of Type 1 diabetes. Patients with IBD have shown clear shift of the gut microfloral composition towards less lactic acid-producing bacteria. In addition, the relative load of some species of colon-associated bacteria such as Bifidobacteria shows little presence in the gut of IBD patients indicating less bacterial-synchronization and disturbed quorum sensing processes in such patients. Interestingly, antibiotics are used in IBD to treat infective complications and to improve symptoms through altering the gut microfloral composition [32].Maintenance of the physical integrity of the gut is essential to limit penetration of harmful bacteria. Dorsal to the epithelial layer in the gastrointestinal tract is a protective mucous gel layer which is altered by the existing microbial colonies. The neutral pH of the epithelium is preserved by the mucin, which creates a gradient to the acidic contents of the gut. It acts as a physical barrier to block microorganisms from adhering to the underlying epithelium and prevents sheer stress on the gut. The spread of harmful xenobiotics through the gut is limited by the mucin, which is normally a thick and viscous layer.
In a germ-free environment the mucous layer is thinner and has a different mucin content and composition. Recent literature has shown that in ulcerative colitis and, to a lesser extent, Crohn's disease are associated with a significant reduction of the protective gut-mucus layer, however, the role of this alteration in the pathogenesis of both diseases remain unclear [33].Localized inflammatory responses are modulated by the gut microfloral bacteria that seek to establish an ideal environment for their growth. The gut microfloral bacteria also alter inflammatory mediators which utilize the lymphatic system for transport, altering sites of inflammation outside the gut.Intercellular interactions can also change gut permeability and are influenced by gut microflora. Zonula occludens are proteins that provide a structural framework to cells and seal the space between them, preventing the movement of ions across the barrier. A number of pathogenic bacteria and parasites target these epithelial cell membranes to increase the gut vulnerability to penetration.
Comparatively, the presence of some beneficial bacteria can increase the expression of zonula occludens at tight junctions, improving epithelial integrity and cell-cell adhesiveness.
It is important to stress the fact that both, the complexity and versatility of gut microflora, remain major challenges to precisely be able to measure the changes in bacterial composition in diseases patients and compare that to healthy ones. In addition, the effect of food, drug consumption, gender and age may also influence gut microfloral composition adding complexity when comparing healthy versus disease states.
To complicate this further, the interaction between bile acids and gut microflora has a significant effect on the density, composition, type, colonization and quorum sensing processes of various strains of gut bacteria, thus, making bile acids (BA) a major component of the bacterial-ecosystem that exists in the gut. This necessitates including bile acids, with when investigating autoimmune-associated disturbances in gut microbiota.
They are known to provide human with health benefits through their endocronological, microfloral, metabolic and other known and unknown effects. Disturbances in bile acids composition and functionality may cause tissue damage and eventual necrosis due to higher than normal concentrations of potent bile acids such as lithocholic acid compared with less potent bile acids such as chenodeoxycholic acid [34]. The nature of the interaction between gut microflora and bile acids is based on the fact that secondary bile acids are solely produced by the action of gut microflora. This interaction between bile acid composition and the composition of gut microflora represents the base of the hypothesized linking between bile acid, gut microflora and energy balance.
However, even though the compositions of bile acids and gut microflora are reported to be different in diabetic patients [35], it is still not clear how these changes directly affect the development and progression of diabetes or its complications. These complications include cardiovascular, tissue necrosis and ulcerations, and metabolic disturbances. Even though the composition of gut microflora has been reported to be different in T1D patients, it may be difficult to quantify or qualify such a difference. Gut microflora interacts closely with the body immune system and has shown to control the immune response to various inflammatory stimuli.
Firstly, by competitive exclusion, where gut microfloral bacteria resist colonization of other 'foreign' bacteria. Secondly, by barrier formation where the microflora forms a physical barrier reducing bacterial translocation by forming a wall surrounding the outside part of the gut enterocytes. Thirdly, gut bacteria can produce bacteriocins and change the pH to create a harsher environment for other invading bacteria to settle in the gut. Fourthly, gut microflora can influence the immune system through its effect on gut enterocytes (quorum sensing) and the innate and adaptive immune system [36, 37].
To understand better the autoimmune-associated disturbances in the gut microflora, there is a definite need to understand the mechanism by which gut microflora interacts with the epithelial mucosa lining up the intestinal tract. Over the last decade, there have been growing interests in studying the mechanism by which enterocytes interact with gut microflora.The epithelial mucosa is inhabited by significant number of various immune cells that work as a link between the gut epithelia and lumen-contents [38].
Thus, T helper cells have a more administrative role where it comes to neutralizing infected cells.
They are essential in B cell antibody class switching, in the activation and growth of cytotoxic T cells, and in maximizing the antibacterial activity of phagocytes such as macrophages [39-41]. After a period of time, T helper cells start expressing CD4 which is a specialized surface protein. So when a body-cell is infected with an antigen, and this cell expresses this antigen on MHC class 2, a CD4 cell will promote the cell interactions and elimination. The lamina propria is a layer of connective tissue that lies adjacent to the epithelium of a mucous membrane.
Many T helper cells, macrophages and IgA-producing plasma cells are present in the lamina propria [4]. Specialized microfold (M) cells of the lymph tissues can be found in the epithelial mucosa in the gut.
M cells play a crucial role in the genesis of systemic immune response by delivering antigenic substrate to the underlying lymphoid tissue where immune responses start.
Although it has been shown that dendritic cells also have the ability to sample antigens directly from the gut lumen, M cells certainly remain the most important antigen-sampling cell and are affected in the autoimmune diseases. Dendritic cells are bone marrow-derived antigen-presenting cells that essentially influence all aspects of innate and acquired immunity (Figure 2). These cells sense the microbes in their milieu through TLRs, and by signalling via different TLRs, generate biological reactions which produce variable responses from excitatory to suppressive. Dendritic cells are heterogeneous inhabitants of the intestine found scattered in all lymphoid compartments and can enter between epithelial cells to taster lumenal bacteria which they can then present to immune cells in the mucosa. In healthy individuals, cytokines and mature T cells suppress ‘exaggerated’ T cell response that may result in unwanted cell damage, apoptosis and death.
Thus, gut microflora in each individual, works as a finger print and exerts a significant control over the immune response to various ‘antigenic’ stimuli.
In addition to the gut microfloral control on the intestinal immunoregulatory system and the mucosal barrier, it is also involved in the pathogenesis of symptoms related to metabolic interactions of the microflora with intestinal contents or intestinal functions such as peristaltic movement [25, 26, 42-44]. Changes in the permeation of the intestine have been strongly associated with various autoimmune diseases such as T1D and IBD. However, the efficacy of probiotic treatment in autoimmune diseases is still under scrutiny and despite excellent progress in studying changes in gut microfloral composition associated with many autoimmune diseases, probiotic therapy has still not shown clear clinical efficacy in treating such conditions.
The reported changes of intestinal permeation seem to indicate weakness of enterocytic tight junctions as well as the integrity of the epithelial mucosa as a whole. During the autoimmune process, inflammation becomes sound resulting in increased mucosal permeability (Figure 1).
This may result in antigens reaching the lamina propria (from the lumen) triggering an autoimmune response.
Animal models suitable for investigating probiotic applications in autoimmune diseasesDuring the process of drug development, various in vivo, ex vivo, in situ and in silico methods can be used. Each method has advantages and disadvantages, and so using more than one method can provide better confirmation of findings. In silico methods can provide an initial insight into a potential drug candidate with predicted high pharmacological activity and good stability, while ex vivo methods can provide more information about a drug’s interaction with living tissue, and are more cost-effective compared with in vivo animal models [49]. In situ methods can better predict drug absorption compared with ex vivo models but in vivo models can provide more comprehensive pharmacokinetic profiles and give a better understanding of drug-tissue interactions [50].
In vivo studies are usually carried out where drug therapeutic formulations are administered to animals in order to investigate short and long term safety, to explore various clinical effects and to study different physicochemical parameters before confirming suitability of the formulation to a disease condition(s). In vivo studies on specialized animal models have allowed a great progress in tailoring research questions towards individualized gene contributions and their effect on the pathogenesis of these diseases.
This has been done using standard inflammatory disease models in transgenic animals and by identifying novel models through the induction of the disease using chemicals. Although there is a surplus of animal models (spontaneous and induced) to study various autoimmune diseases, there is no ideal or standard model for studying the effect of probiotics on each condition [52-55]. However, future research is needed, to compare the effect of probiotics on various animal models of ADs.
An ideal animal model should represent a specific medical condition in terms of disease development, pathophysiology, biological disturbances and short & long term complications [56-58]. The current therapeutics for ADs are inadequate, which necessitates further drug development and in vivo trials. Clinical translation of AD’s pathophysiology and clinical manifestations, from animal to human, has been limited and rather difficult. This is because very little is known about the pathophysiology and prognosis of such conditions; the extent of heterogeneity, polymorphism, genetic distance, the exact site of initial immune response (gut, lymph nodes, blood, brain or?), and ‘potential’ triggering antigens.
To complicate this further, different Ads have different signs and symptoms and thus, one animal model is unlikely to be always suitable for all conditions. Creating a suitable animal model for ADs requires the ability to accurately translate the findings to human. The nonobese diabetic (NOD) mouse is considered the ‘standard’ animal model of the disease.
Other models are induction models of rats, mice and hamsters using alloxan or streptozotocin to destroy pancreatic beta cells and induce T1D. The NOD mouse represents the best spontaneous model for a human autoimmune disease, in particular, T1D.
NOD mouse model allows the investigation of various immunointerventions that can be used in human T1D. However, the development of T1D in NOD mouse takes place quickly and can produce a significant inflammatory condition that may over-respond to immunomanipulation and exaggerate the effect of a treatment.
Also, the incidence of T1D is different between males and females in this model while the incidence is the same in males and females in human. Many therapeutics that showed good efficacy in this model failed to achieve similar results in T1D human subjects [60].
Having said that and regardless of how different this model is, from the 'true' human TID, NOD mouse remains the most representative of human T1D.
Interestingly, in a recently published study, the incidence of T1D was much higher, when the mice were maintained in a germ-free environment suggesting direct connection between gut microflora and the development of T1D [61, 62].Overall, a suitable animal model for human AD should ideally be easy to breed and handle, and can accommodate various medical conditions that may come about or be associated with the condition it is representing. Thus, extrapolation of its findings to human should be easily done, and with great accuracy and precision.4. The influence of gut microflora on the development of autoimmune diseasesIn many autoimmune diseases, the gut microfloral composition is different than that of healthy individuals. However, the cause of this change of composition and whether this change is a contributing factor to the development of the disease remain unclear.
Probiotic treatment has demonstrated potential benefits in many Ads, assumingly, through normalizing such changes in the gut microfloral composition.
Interestingly, the literature suggests that the effect of probiotic treatment on ADs’ development and progression may be brought about through the effect on the expression and functionality of certain protein transporters.
Recent publications suggest that many transporters have their expression and functionality altered in the autoimmune disease; T1D [23, 27, 72]. The exact mechanism associating the change in transporters and diabetes’ development is still unknown but there are few assumptions to explain such an interaction. The first assumption is that some ADs, start with a direct insult in the gut, initiating a disturbance in the gut microflora and a consequent disturbed bile flow.
This results in an altered bile feedback mechanisms and a change in the expression of protein transporters responsible for bile enterohepatic recirculation. The second assumption is that disturbance in protein transporters expression and functionality, caused by a genetic mutation, produces a disturbance in enterocytic-microfloral interactions triggering an inflammatory response. The third assumption is that the functionality of the immune system is altered (due to either an insult in the gut or genetic mutation). This alters the composition of gut microflora resulting in initiating of inflammation reaching various body tissues causing systemic inflammatory response triggering an autoimmune disorder and eventuating in autoimmune systematic response. In all these assumptions, genetic susceptibility is expected, and contributes further to the disease development and progression.
The above assumptions were based on the work of the authors as well as careful evaluation of the literature. In recent publications, alterations in the functionality of some transporters have been linked directly to the development of some autoimmune diseases such as diabetes.
In addition, the enterohepatic recirculation of bile acids has also been related, by association, since secondary bile acids are solely produced by the action of gut microflora [13]. Bile salts’ output in diabetic animals was high compared with healthy, and the expression of Mdr2 was also high after STZ treatment [63].
In another study, a mutation in Zinc transporter 8 (ZT8) located in beta cells, is implicated in the dysregulation of insulin transport and release, and an exacerbation of the inflammatory response leading to T1D. In this study, ZT8 was considered as an autoantigen resulting in the stimulation and production of beta cells autoantibodies and T1D development [64]. Hyperglyemia itself directly reduced the activity of Mdr1 suggesting a clear association between pre-T1D hyperglycemia and disturbances in protein transporters [66]. In another recent study, the effect of STZ on cation protein transporters was reported, interestingly, at different levels of protein synthesis; transcriptional and posttranscriptional depending on the type of the transporters affected [67]. However, some studies suggest a diabetic influence is stronger on enzymatic activities than on protein transporters with the enzymatic influence being the cause of exacerbation of inflammation and development of the disease [68].
The impairment of protein transporters functionality, reported in the diabetic animals can take place either by reduced protein expression or reduced action. When glucose protein transporters in the blood brain barrier were studied under chronic hyperglycemia, their concentrations remain constant but functionality and glucose intake were impaired [69]. However, under acute hyperglycemia induced by STZ, their concentration decreased suggesting different response at different stages of the disease [70-72].
Accordingly, protein transporters have shown strong association with diabetes development and progression as well as diabetic complications.
Although there is some evidence suggesting that unrelated infections can result in the induction of organ specific autoimmunity [73], there is abundant epidemiological, clinical, and experimental evidence linking similar and closely related infectious agents with autoimmune diseases. Accordingly, the most acceptable hypothesis explaining how infectious agents cause autoimmunity is “molecular mimicry”. Molecular mimicry directly invokes the specificity of the immune response to the resultant breakdown of tolerance. It proposes that microbial peptides have structural similarities to self-peptides and are therefore involved in the activation of autoreactive immune cells [74, 75]. Peptides, primarily, heat shock proteins (HSPs), have been implicated in autoimmunity [76, 77].HSPs are a highly conserved family of proteins with significant structural homology between humans and bacteria.
HSPs are located on almost all subcellular and cellular membranes and their numbers are induced in response to high temperatures and stress. HSPs function as molecular chaperons which are instrumental for signalling and protein trafficking. HSPs are believed to act through the activation of Toll-like receptors (TLRs) which trigger the expression of several genes that are involved in immune responses.TLRs are only present in vertebrates and at least 11 TLRs are currently known. Distinct TLRs are differentially distributed within cells: TLR1, TLR2, TLR4, TLR5, TLR6, TLR10 and TLR11 are transmembrane proteins expressed on cell surfaces that contain extracellular domains rich in leucine that interact with pathogenic peptides, whereas TLR3, TLR7, TLR8 and TLR9 are primarily distributed on the membranes of intracellular compartments such as endosomes [78, 79]. They are proteins on intestinal membranes that bind to pathogen-associated molecular patterns (PAMPs). After binding they release nuclear factor-kappa B (NF-kB) which moves into the cell nucleus and stimulates the release of pro-inflammatory mediators to target pathogens [80, 81].
Gut microfloral bacteria can directly trigger TLRs through adhering to the epithelial mucosa.
As the human gut contains such large volumes of beneficial bacteria, they constantly trigger the TLRs.


This leads to an eventual attenuation in the TLR response [82-84], (see Figure 2).Although both pathogenic and probiotic bacteria regulate immunity via activation of TLRs, they do not usually trigger the same pathogenic inflammatory responses.
Therefore, it is of biological and clinical importance to understand how very similar molecular proteins (HSPs) released by both commensal and pathogenic bacteria can trigger different responses by stimulating the same cellular receptors. One of the reasons for this may be that although the proteins are very similar they are not identical and thus they may stimulate the receptors in different ways to either produce a pro-inflammatory or an anti-inflammatory response.
Another possibility is that the slight differences in the peptides allow them to bind to different TLRs leading to dissimilar responses.
A third reason might be that more than one TLR is involved and that the effects seen are a synergistic effect depending on which TLRs are involved. TLR2 recognizes a variety of microbial components which include lipopeptides and peptidoglycan as well as lipopolysaccharides (LPS) from non-enterobacteria. TLR4 is an essential receptor for (LPS) recognition [85-87] and it has been shown to be involved in the recognition of endogenous heat shock proteins, eg HSP60 and HSP70. TLR2 appears to form a heterophilic dimer with TLR1 or TLR6 but other TLRs are believed to form homodimers. TLR1 and TLR6 that are functionally associated with TLR2 allow for the discrimination between diacyl and triacyl lipopeptides. Dimerisation of TLRs triggers activation of signalling pathways through the cell and into the nucleus. However, different gene expression profiles are triggered depending on which TLRs and TLR combinations are activated. Dendritic cells are believed to be critical to the balance between tolerance and active immunity. Intestinal Dendritic cells are excessively activated in IBD as well as other autoimmune diseases which indirectly links the gut microfloral disturbances with the initiation or the progression of the disease (see Figure 2). Thus, the influence of disturbances in normal gut microflora may be indirectly linked to the initiation, development, progression and prognosis of many of the autoimmune disease. Such disturbances have been linked to changes in the expression and functionality of protein transporters in and outside the gastrointestinal tract. These disturbances have also been linked to changes in the composition and functionality of bile acids and many physiological and biochemical feedback mechanisms that showed clear impact on the stability, performance and efficiency of the immune system and its associated lymph tissues. However, many studies may show a significant impact or the lack of it, when trying to rectify these disturbances through the treatment with probiotics, making the influence of gut microflora on the development and progress of autoimmune disease difficult to clearly explain. Consequently, a direct influence of normal microfloral composition on the body’s inflammatory response has been demonstrated in the literature. This directs further research towards investigating how the gut microflora can potentially control the immune system to the extent where its manipulation may delay or even prevent the initiation of the inflammatory response leading to the clinical signs and symptoms of the immune disease. The effect of probiotics on autoimmune-associated inflammationBacterial gut-microflora live in an ecosystem, where each bacterial colony is part of a bacterial strain that colonizes the gut, and interacts with each other, as well as, with other gut-bacterial strains.
The nature of this interaction is being currently studied at many scientific labs worldwide, and evidence of cross-talking continues to emerge.
Bacterial cross-talking process involves polypeptide-based signals being secreted by various bacteria that influence the protein expression and functionality in other bacteria [25, 88].
This means that bacteria can influence the expressions and functionality of various proteins and membrane-transporters of other bacteria, via changing the gut concentrations of certain polypeptides. This can be brought about through the induction or suppression of membrane-transporters or through the process of direct-signalling [38]. In matter of fact, sequencing of human faecal samples has identified over 5000 different active gut-bacteria, with known metabolic activities [24].
Infants in the womb are mainly germ-free with the exception of some microbes that may be acquired through the swallowing of the amniotic fluid. The type and variance of these microbes and the role each gut-bacterial strain plays in initial gut-ecosystem development is still not completely understood. The next exposure to microflora takes place during birth when infants inherit a bacterial profile from their mother that shapes the composition of the matured gut. This profile of bacteria differs with type of delivery (vaginal or caesarean), time taken for the membrane of the amniotic sac to rupture, gestational age and use of antibiotics during labour. The human gut undergoes continuous maturation over many years, and has a shifting microbe population that varies between individuals and their exposure to family members, especially siblings, the sanitation of living conditions, and food and drink. The balance of different bacteria stabilises as people age but is still affected by factors including diet, location, antibiotic use and radiation exposure in adults. Autoimmune disease such as diabetes, show substantial inflammatory response, and bile acids disturbances can cause chemical unbalance that has been linked to poor tissue sensitivity to insulin [108], rise in the levels of reactive radicals in the blood [109], poor enterohepatic recirculation and dysfunctional protein-transporters in the gut that is negatively affecting liver detoxification and performance [110]. Accordingly, future AD-therapy should not only focus on rectifying physiological imbalance but also in targeting the disturbances in bile acids composition, protein transporters and overall the inflammation cascade initiated in the gut. This can be achieved through normalizing the composition of gut microflora and bile acids, gut immune-response and microflora-epithelial interactions towards maintaining normal biochemical reactions and healthy body physiology. Physiological features of human development including the innate and adaptive immunity, immune tolerance, bioavailability of nutrients, and intestinal barrier functions, are directly related to the composition and functionality of the human microflora.
Microflora modifications may take place due to antibiotics consumption, prebiotic and probiotics administration and the use of drugs which affect gastric motility resulting in changes in gastric pH and gut-emptying rate.
These modifications have been shown to be significantly profound in diabetic subjects resulting in the reduction of the percentage of good bacteria, the increase of the percentage of bad bacteria and yeasts and the consequent increase in the percentage of toxic bile salts such as lithocholic acid. This can also contribute to the higher incidence of gall stones and liver necrosis reported in diabetic patients.
Accordingly, probiotics can introduce missing microbial components with known beneficial functions for the human host, while prebiotics can enhance the proliferation of beneficial microbes or probiotics, resulting in sustainable changes in the human microflora.
Symbiotic relationship between probiotics and prebiotic administration is expected to exert a synergistic effect and in the right dose, may normalize and even reverse dysbiosis-associated complications. Continuous exposure to bacteria can induce mucin secretion and change the structure of the mucous layer which can play a role in maintaining mucus thickness and its protective effects.
In a recent in vivo study, Wistar rats were administered a probiotic formulation (VSL#3) daily for seven days.
After probiotic treatment, basal luminal mucin content increased by 60% which has been linked to better protective effect and substantial stimulation of mucin secretion at the level of DNA-gene expression [90-93]. The significance and magnitude of the effect of host genetics on gut microfloral composition and functionality is difficult to accurately determine [94, 95]. It is generally agreed on that initial colonisation has the greatest effect on the lifelong bacterial types and functionality. Accordingly, it is expected that family members with shared genetic factors are likely to share the same initial colonisation similarities between their bacterial types. However, when the similarity of bacterial populations was compared between identical twins, non-identical twins and siblings, it was found that identical twins had significantly closer microflora compositions while others did not [96]. Other studies have observed bacteria modification after changes in host allele types, which also indicates some genetic effects but evidence remains controversial. Thus, it is clear that genetics do influence bacterial types in the gut, as does diet, environment and a multitude of other factors.
Accurate definition to the contribution of each factor to the types and functionality of gut microflora remains to be studied. They ferment and break down otherwise indigestible food components, thus, making additional nutrients available to the human host. Gut-associated lymphoid tissues are collections of immune cells in lymphoid tissue in the gastrointestinal tract [98].
Dendritic cells function as messengers which present endocytosed antigens to the Peyer’s patches or mesenteric lymph nodes to prime T-cells into effector cells [100]. If the antigens are presented to the mesenteric lymph nodes, the effector cells are released into systemic circulation via the efferent lymphatic system, leading to an inflammatory response from central lymph nodes. Through effects on the dendritic cell intermediary, bacteria can modulate T-cell regulators which can lead to alter systemic inflammation via lymphatic systems. Gut growth in animal studies where mice are raised in a microbe free environment shows a different intestinal structure compared to normal gut growth and the amount of gut-associated lymphoid tissue is reduced [101, 102]. This results in reduced gut microfloral differentiation between beneficial and pathogenic bacteria, bringing about a significant reduction in the area of the gut which can launch an innate immune response and decreases the communication of antigen information to central lymph nodes. This makes the entire body more vulnerable to harmful bacteria passing through the gut epithelium unnoticed [103-105].In mice, a disturbed TLR-pathway results in compromised TLR signalling which results in any intestinal injury being met with an exaggerated response [81, 106-108].
A down-regulated TLR pathway caused by dysbiosis could cause a similar inflammatory process, making commensal bacteria potentially protective against IBD [109, 110]. This indicates the necessity of the TLR conditioning to develop an immune tolerance to bacterial threats in the gut.
Bacteria in the gut can also bind to PAMPs to deliberately initiate an inflammatory response to signal the presence of invading pathogens.
Overall, these changes to inflammatory signalling and response based on interactions with gut microfloral bacteria are numerous and varied in mechanism. This indicates a complex relationship between the innate immune system and gut microflora where both parties are adaptive to the other, rather than static in response.Many autoimmune and inflammatory diseases have shown positive response to probiotic and prebiotic treatments.
The composition of the intestinal microflora may even affect mammalian physiology outside the gastrointestinal tract [111].
Recent studies have shown significant changes in gut microfloral and bile acid compositions in T1D [28, 43].
Thus, it is clear that our symbiotic microflora award many metabolic capabilities that our mammalian genomes lack [112], and so therapeutics that target microfloral modulation may prove rewarding. Gut microflora has been shown to play a major rule in controlling the inflammatory response of the host immune system through direct and indirect bacteria-bacteria and bacteria-host interactions. These interactions include physical and metabolic functions of the gut microfloral bacteria, which protect the intestinal tract from foreign pathogenic bacteria, eliminate the presence of unwanted bacteria through producing bacteriocins and other chemicals, and inform the gut epithelium and the host immune system about whether a local inflammatory response is needed [37, 113]. The induction of IgA secretion to protect against infection, triggers localized inflammatory responses, neutralizing T-helper (Th) cell response and also contributing to the induction or inhibition of generalized mucosal immune responses. In recent studies, gut-associated dendritic cells in the lamina propria can extend their appendices reaching the gut mucosa and using their Toll-like receptors (TLR) 2 and 4, to sample bacterial metabolites [114, 115].
Interestingly, some microfloral bacteria can actually cross enterocytic microfolds and interact with antigen presenting immune cells in mesenteric lymph nodes to activate naive plasma cells into IgA-producing B cells [116].
IgA coats the intestinal mucosa and control further bacterial penetration thus protecting the host from potential pathogenic bacteria. Even more interestingly, gut microflora bacteria have shown ability to not only initiate an inflammatory response but also to control and inhibit such a response. Some microfloral bacteria or their metabolites can interact with the intracellular receptor TLR-9, to which the bacteria activates T cells through the production of potent anti-inflammatory cytokines such as IL-10 [117, 118].
Microfloral bacteria can also produce small molecules that can enter intestinal epithelial cells to inhibit activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB) [119].
Moreover, prolonged exposure to bacterial endotoxins, in particular, LPS (which interacts with TLR 2 and 4) can activate intracellular anti-inflammatory associated proteins that result in an overall anti-inflammatory effect [120]. Such gut bacterial-host interactions are critical in maintaining a balanced and effective immune response to various infections while maintaining control over prolonged or chronic inflammation and reducing the overstimulation of the host immune system. Recent evidence suggests that a particular gut microfloral community may favour occurrence of the metabolic diseases. It is well know that the composition of gut microflora changes with diet and also as we age [121, 122]. In one study, a high fat diet was associated with higher endotoxaemia and a lowering of bifidobacterium species in mice cecum [123-125]. In a follow up study, the administration of prebiotics, in particular, oligofructose, to mice given high fat diet, restored the reduced quantity of bifidobacterium. This also resulted in reducing metabolic endotoxaemia, the inflammatory tone and slowing the development of diabetes. In this study and compared with control mice on chow diet, high fat diet significantly reduced intestinal Gram negative and Gram positive gut bacteria, increased endotoxaemia and diabetes-associated inflammation. However, when diabetic mice on high fat diet were given oligofructose, metabolic normalization took place including the quantity of gut bifidobacteria. In these mice, multiple correlation analyses showed that endotoxaemia negatively correlated with bifidobacteria quantity [126, 127]. By the same token, bifidobacterium quantity significantly and positively correlated with improved glucose tolerance, glucose-induced insulin secretion and normalised inflammatory tone (decreased endotoxaemia and plasma and adipose tissue proinflammatory cytokines) [123-125]. In general, the level of microfloral diversity and gut bifidobacteria in human, relate to health status and both decrease with age [128, 129].6.
The potential applications of probiotics in autoimmune diseasesProbiotics have been shown to be beneficial in wide range of conditions including infections, allergies, and metabolic disorders such as diabetes mellitus, ulcerative colitis and Crohn’s disease [130-132].
When discussing therapeutic applications in AD, the use of probiotics is an area of growing interest, not just as an adjunct therapy but also as a mainstream treatment aiming at normalizing the disturbed gut-microfloral composition, as well as, directly relieving signs and symptoms of the disease. In order to design a probiotic formulation that targets disease-associated disturbances in gut microflora, a better and more detailed understanding of these disturbances is necessary. Better understanding of microfloral composition in the gut can be achieved through cell-culturing and protein-based assays that analyse the nature, type and quantity of various bacteria that exist in the gut. Type 1 diabetes and probioticsProbiotic administration in animal models of Type 1 diabetes has shown great potentials. Combinations of different bacterial strains can be used [133] but a mixture of Lactobacilli and Bifidobacteria is a common choice [20-23, 26, 42, 92, 134-136]There are reports in the literature that probiotic treatment can be useful in diabetes [28] but there is little explanation of the mechanisms involved. The initial site of diabetogenic cells has been hypothesized to be in the gut whereas pancreatic lymph nodes serve as the site of amplification of the autoimmune response [137]. Treatment with Bifidobacteria and Lactobacilli has been shown to normalize the composition of the gut flora in children with T1D [131, 138]. In addition, the administration of Lactobacilli to alloxan-induced diabetic mice prolonged their survival [139, 140] and administration to non-obese diabetic (NOD, a rodent model of T1D) mice inhibited diabetes development possibly by the regulation of the host immune response and reduction of nitric oxide production [140]. Furthermore, the administration of a mixture of Bifidobacteria, Lactobacilli and Streptococci to NOD mice was protective against T1D development postulated to be through induction of interleukins IL4 and IL10 [141]. This can result in a bigger population of bacteria in the gut and a subsequent rise in the concentration of secondary bile acids [142, 143] such as lithocholic acid [144, 145]. In addition, the disturbed bile acid composition in T1D (8) is strongly linked with autoimmune and liver diseases. The administration of Lactobacilli and Bifidobacteria may restore the bile acid composition [146, 147].
It is important to select the right probiotic species based on efficacy, stability in the gut (bile and pH tolerability) and long term safety. For example, some probiotic-bacterial cells have been examined for stability as well as efficacy in various autoimmune diseases.
Inflammatory bowel diseases and probioticsIn IBD such as UC colitis, there is a substantial inflammatory component with atypical type 2 T-helper cell (Th2) activation. Th2 are activated by the presence of antigens and then direct other immune cells in the body. In UC they can become overly sensitised and secrete interleukin-13, an inflammatory mediator [151]. This drives T-cells not normally present in the colon to migrate there and makes the colon mucosa more sensitive to commensal bacteria which drives further inflammatory responses [152].Naive CD4 T cells differentiate into Th1 or Th2 effector T cells on activation by antigen-presenting cells (see Figure 4).
Th1 and Th2 cells carry out distinct antigen specific adaptive immune functions; Th1 cells mediate cellular immunity against intracellular pathogens, whereas Th2 cells enable humoral immunity and immunity against extracellular pathogens. The effector functions of Th1 cells are exerted in part by production of interferon (IFN)-? and those of Th2 cells by interleukins including IL4.
Inappropriate regulation of Th1 and Th2 cell functions can cause autoimmune diseases.In IBD, UC in particular, as with other inflammatory conditions, the production of immunoglobulins is elevated. Immunoglobulins, or antigens, bind to antibodies to encourage an immune response to the antigen while limiting the harm the antigen can do.
That antigen is also present in the eyes, skin and joints and inflammatory responses there can cause the extraintestinal symptoms associated with UC, including peripheral arthritis, erythema nodosum, iritis, uveitis and thromboembolism [153].The identification of a causative UC pathogen would greatly simplify diagnosis and new treatment identification. Three broad studies used sequenced bacteria from the human gut to try and identify a healthy gut microbial profile. When the bacteria strains were divided by phylogenetic type it was found that 98% of bacteria were part of four phyla [154-156]. Another study compared this control data to samples from patients with Crohn’s disease and UC. Two-thirds and three-quarters of the diseased samples, respectively, had the same bacterial balance as healthy controls. In the other IBD samples there was no consistency in the atypical bacterial groups, indicating that although dysbiosis is present there are no single causative bacteria [154]. Unfortunately, it is still unknown whether the dysbiosis precipitates gut inflammation or if another cause initiates the disease and dysbiosis occurs due to the inflammatory changes [157]It has been shown that patients with UC display an increased microflora density [151] meaning the total population of bacteria in the colon is increased. In one study the number of bacteria in colon biopsies taken during endoscopy from newly diagnosed and untreated UC patients was double that of healthy controls [158]. The samples from UC patients also showed a thinner and less sulphated mucosal layer of the gut epithelium [159] which could support the increased bacterial levels through a lessened mucus flow to dislodge bacteria or an improved nutritional role from less sulphate.VSL#3 is a high dose probiotic mixture that shows how information from multiple trials and in vitro studies can be brought together. Considering how new data fits into the probiotic profile established from previous investigations can help highlight any challenges to existing assumptions.
Alternatively, when study results are replicated by different research centres the significance of the findings is increased.
This reflective process should develop an understanding of the probiotic that is based on clinical evidence. VSL#3 contains a combination of three strains of bifidobacterium, four strains of lactobacilli and one strain of streptococcus salivarius.
A trial in 1999, shortly after the probiotic was developed, tested faecal samples of 20 UC patients to determine changes in bacterial concentrations when VSL#3 was administered with no other treatment.
An increase in the bacterial numbers of strains found in the probiotic was observed in all patients from the 20th day of treatment and remained stable.
This established that the probiotic could colonise the gut and encouraged further clinical trials [160]. VSL#3 was then trialled repeatedly in small studies which had similar conclusions regarding safety and efficacy.
The studies showed a low number of reported side effects which were consistently mild, so safety in the trialled patient types was assumed. The outcomes from the trials were encouraging as the probiotic treated groups usually showed an improvement in disease state [92, 161-166]. This identified VSL#3 as a feasible new UC treatment but a large, randomised, placebo controlled study was needed to verify results [167].



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