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Probiotics in health maintenance and disease prevention requirements,best probiotics on the market 2015 birmingham,what enzymes digest milk anymore - PDF 2016

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Every year in the United States approximately 200,000 people die from pulmonary infections, such as influenza and pneumonia, or from lung disease that is exacerbated by pulmonary infection.
Respiratory tract infectious diseases, such as influenza and pneumonia, result in the death of 3·2 million people annually worldwide (WHO, 2014). Alterations of the intestinal microbiota not only affect the growth of opportunistic pathogens but can have a broad impact on immune status and function within the host (Hooper et al., 2012). Commensal microorganisms modulate host immunity not only in the intestinal tract but at distal sites as well (Kieper et al., 2005). Expansion and differentiation of extra-intestinal T cell populations are meditated by the intestinal microbiota (Kieper et al., 2005). Development of oral tolerance occurs following oral administration of antigen and represents a local and systemic immunological state of immune unresponsiveness to a subsequent antigen challenge. Dietary fermentable fiber content changes the composition of the GI microbiota, in particular by altering the ratio of Firmicutes to Bacteroidetes. While the all of the direct mechanistic contributions of the GI microbiota on systemic immunity beyond the intestinal mucosa remain to be determined, these studies demonstrate that commensal bacteria can impact host immunity beyond the GI tract.
It is important to understand the cross-talk and collaboration between the GI tract and the respiratory tract at both an immune and microbial level. It is evident that the intestinal microbiota plays a crucial role in the regulation and immune response to respiratory viral infections such as influenza (Ichinohe et al., 2011). Similar observations regarding the critical role of the intestinal microbiota in the regulation and immune response to respiratory bacterial infections have also been made (Fagundes et al., 2012). Gut-derived sepsis is the process during which gut-derived proinflammatory microbial and non-microbial factors induce or enhance a systemic inflammatory response syndrome (SIRS), acute respiratory distress syndrome (ARDS), or multiple organ dysfunction syndrome (MODS). This means that you will not need to remember your user name and password in the future and you will be able to login with the account you choose to sync, with the click of a button. This page doesn't support Internet Explorer 6, 7 and 8.Please upgrade your browser or activate Google Chrome Frame to improve your experience. Most of the current therapies used in the treatment and management of these diseases are suboptimal as antibiotic resistance, efficacy, and toxicity have been difficult to overcome (Keely et al., 2011).
Evolution of an individual's microbiota begins shortly after birth cumulating in a stable adult microbiota by the age of two (Foxx-Orenstein and Chey, 2012).
The impact of the GI microbiota on host mucosal immunity has been studied extensively in germ-free mice (mice without any intestinal microbiota). The intestinal microbiota affects systemic immune responses by modulation of several key pathways; expansion of extra-intestinal T cell populations, production of short-chain fatty acids, development of oral tolerance, and control of inflammation. Several recent studies have shown that the intestinal microbiota is critical for maintenance of T cell subsets that are important for systemic immunity. Low doses of antigen favor active suppression, whereas higher doses favor clonal deletion of antigen-specific T cells. Alteration of the ratio of Firmicutes to Bacteroidetes directly affect how the gut microbiota metabolize fiber, consequently increasing or decreasing the concentration of circulating short-chain fatty acids (SCFAs).
Table 1 summarizes our current understanding of the effect of the intestinal microbiota on systemic immunity. Numerous studies have shown that fluids, particles, or even microorganisms deposited into the nasal cavity of mice can also be found in the GI tract a short time later (Southam et al., 2002). Th2 cells are characterized by their ability to produce IL-4, IL-5, IL-9, and IL-13 (McLoughlin and Mills, 2011). A recent study from Ichinohe and co-workers demonstrated that the GI microbiota directly influenced virus-specific CD4 and CD8 T cell subsets in experimentally infected mice (Ichinohe et al., 2011).
Therefore, understanding the mechanistic basis for host defense against infection and regulation of immune processes involved in asthma are crucial for the development of novel therapeutic strategies. Infection of the respiratory tract represents a breakdown of the host's immune defenses. This microbial community includes autochthonous (permanent inhabitants) and allochthonous (transient inhabitants) microorganisms. The intestinal microbiota is required for expansion of CD4+ T cells, regulatory T cells, Th1 or Th2 responses, and Th17 T cells.
For example, germ-free mice with chemically induced colitis exhibit markedly attenuated pathological signs of colitis and restoration of the intestinal microbiota prevents the attenuation. A model for the regulatory influence of the gastrointestinal microbiota on systemic immune responses. Treatment of mice with different antibiotic regimens revealed a population of neomycin-sensitive commensal organisms associated with a protective immune response in the lung following influenza infection.
The identification, characterization, and manipulation of immune regulatory networks in the lung represents one of the biggest challenges in treatment of lung associated disease.
In addition, non-infections respiratory diseases are the third and fifth (infections respiratory diseases are the fourth) leading causes of death worldwide (WHO, 2014). Microbiota of the human GI tract contains bacterial (microbiota), viral (virome), and fungal (mycobiota) species.
The specific microbial molecules or components that inform host immune development are still being discovered and characterized. For example, colonization of germ-free mice with Bacteroides fragilis that synthesize PSA results in a higher number of circulating CD4+ T cells and levels of circulating Th1 cells compared to mice colonized with B.
Further, individuals with impaired intestinal permeability often have dysfunctional oral tolerance. More precisely, SCFAs, especially butyrate, seem to exert broad anti-inflammatory activities by affecting immune cell migration, adhesion, cytokine expression, as well as, cellular proliferation, activation, and apoptosis through the activation of signaling pathways (NF-κB) and inhibition of histone deacetylase.
This suggests that the intestinal microbiota is crucial for modulating the host's ability to control inflammation.
Therefore, the GI tract will ultimately be exposed to any pathogen or antigen that is introduced into the respiratory system.
Furthermore, injection of TLR ligands, either locally in the lung or at distal sites, rescued the immune impairment in the antibiotic-treated mice. Germ-free mice were highly susceptible to pulmonary infection with the bacterial pathogen Klebsiella pneumonia. However, any surviving bacteria, cell wall fragments, or protein components of the dead bacteria that escape macrophage containment together with cytokines and chemokines produced in the gut, travel along the mesenteric lymphatics to the cisterna chyli.
Recent evidence suggests that the gastrointestinal (GI) microbiota plays a key role in immune adaptation and initiation in the GI tract as well as at other distal mucosal sites, such as the lung. Understanding the mechanisms that mediate cross-talk between the gastrointestinal (GI) tract and lung defenses and how this interaction facilitates optimal lung health is of growing interest. These include the mucus layer, epithelial antibacterial proteins, and IgA secreted by lamina propria plasma cells.
Impaired intestinal permeability also leads to inadequate production of IgE and recruitment of mast cells in the GI mucosa.


In addition, histone deacetylase inhibitors enhance the numbers and function of Treg cells (Meijer et al., 2010).
This also suggests that the mucosal immune system of the GI tract may serve as a primary sensor of foreign antigens and organisms from the environment. The DC then promote the proliferation and expansion of various T cell subsets in response to antigens. These products then enter into the systemic circulation through the left subclavian vein, via the thoracic duct. This review explores the current research describing the role of the GI microbiota in the regulation of pulmonary immune responses. More specifically, the role of the GI microbiota in mediating, maintaining, and regulating this cross-talk represents an exciting area of research that is poised to aid in the development of novel treatment and management strategies for lung disease. Compartmentalization is accomplished by unique anatomic adaptations that limit commensal bacterial exposure to the immune system. While, colonization of gnotobiotic mice with a cocktail of mouse derived Clostridial strains enhances anti-inflammatory signaling by directing the expansion of lamina propria and systemic regulatory T cells (Treg) with an associated increase in IL-10 secretion (Atarashi et al., 2011).
Individuals suffering from these conditions exhibit enhanced IgE-CD23-mediated transport across the mucosa and increased levels of inflammatory mediators, such as proteases and cytokines, which further affect intestinal permeability. The shifts in the intestinal microbiota populations were also accompanied by increased levels of fecal calprotectin and plasma C-reactive protein, which suggest that the intestinal microbiota alterations found in obese humans are associated with local and systemic inflammation and that the obesity-related microbiota has a proinflammatory effect (Verdam et al., 2013).
This suggests that the intestinal microbiota provides microbial signals or determinants that are critical for immune priming and shaping the response to viral pneumonia. Access to the pulmonary circulation leads to uncontrolled activation of alveolar macrophages leading to acute lung injury or ARDS and then MODS (Senthil et al., 2006). Figure 1 highlights a current overview of understanding of how the GI microbiota shape immune responses and how the host immune system shapes the GI microbiota.
This leads to an increase in the leakage of allergens and hence contributes to perpetuate the inflammatory reaction (Perrier and Corthésy, 2011). Finally, Biagi and co-workers found that by evaluating the correlation between systemic inflammation and the fecal microbiota that about 9% of the variable microbiota was related to the increased levels of pro-inflammatory cytokines IL-6 and IL-8 (Biagi et al., 2010).
We have also provided a summary our current understanding of the effect of the intestinal microbiota on pulmonary health in Table 2. This significantly altered the composition of the intestinal microbiota (Noverr et al., 2004). However, it is estimated that roughly 30-40 species dominate this niche, with bacteria from the genera Bacteroides, Bifidobacterium, Eubacterium, Fusobacterium, Clostridium, and Lactobacillus highly represented (McLoughlin and Mills, 2011). The loaded DCs traffic to the mesenteric lymph nodes through the intestinal lymphatic but do not migrate to distal tissues.
Further, Cassani and colleagues recently observed defective oral tolerance in CCR9-deficient mice (CCR9 targets T cells to the small intestine) and that defective oral tolerance in CCR9-deficieint mice could be restored by transfer of wild-type T cells (Cassani et al., 2011). Furusawa and colleges also demonstrated that treatment of naive T cells under the Treg-cell-polarizing conditions with butyrate enhanced histone H3 acetylation in the promoter and conserved non-coding sequence regions of the Foxp3 locus, which they proposed may be the possible mechanism for how microbial-derived butyrate regulates the differentiation of Treg cells (Walton et al., 2006). All of the taxa that showed a slightly positive correlation with either IL-6 or IL-8 belonged to the phylum Proteobacteria (Biagi et al., 2010).
Disruptions in the intestinal microbiota (dysbiosis) lead to impaired proliferation and expansion of T cell subsets, increased inflammation, and loss or imbalance of bacterial metabolites, all of which can have a negative impact on health and systemic immune response.
This compartmentalizes live bacteria and induction of immune responses to the mucosal immune system. However, Pabst and co-workers found that CCR9-deficient mice developed normal oral tolerance to ovalbumin. Increased levels of butyrate also induce the expression of IL-10, which influence the balance between Th1, cytotoxic CD8+ T cells and Treg cells. The intestinal microbiota also has many inflammation-suppressing fractions, which function to; counteract some of the inflammatory bacteria, decrease the inflammatory tone of the system, improve the barrier function of the GI mucosa, and prevent inflammation-inducing components from translocating into the body (Hakansson and Molin, 2011). This suggests that alterations in the GI flora can facilitate an immunological state that is predisposed to respiratory allergies. Germ-free mice that were conventionalized (normal mouse intestinal flora has been restored) had significantly less K. Many environmental factors will drastically alter the normal intestinal microbiota (Noverr and Huffnagle, 2004). Induced B cells and T cell subsets recirculate through the lymphatic and the bloodstream back to mucosal sites, where B cells differentiate into IgA-secreting plasma cells. Pabst and co-workers suggest that these differences may be due to the differences in individual strains of CCR9-deficient mice, or that differences in the composition of the microbiota may influence the impact of CCR9 on oral tolerance (Pabst and Mowat, 2012). There is a growing interest in understanding other T cell subsets in the development of allergy and asthma, specifically the role of Th17 cells and Th9 cells, which may be impacted by GI microbes (Forsythe, 2014). This theory assumes a three-way partnership among the intestinal epithelium, immune tissues, and the endogenous microflora of the gut. Trompette and colleagues found that mice fed a high-fiber diet had increased circulating levels of SCFAs and were protected against allergic inflammation in the lung, whereas a low-fiber diet decreased levels of SCFAs and increased allergic airway disease. By far, the most studied inflammation-suppressing taxa of the GI microbiota are from the genera of Lactobacillus and Bifidobacterium.
In addition, Vital and colleagues examined the associations between the intestinal microbiota and allergic airway disease in both young and old mice that were sensitized and challenged with house dust mite. Within this three dimensional relationship, each factor modifies the others through crosstalk.
Yet, numerous studies have demonstrated that the intestinal microbiota has a profound effects on the immune system. Specifically, increased levels of SFAs lead to enhanced generation of dendritic cell precursors and subsequent seeding of the lungs by DCs with high phagocytic capacity, which was accompanied by an impaired ability to promote Th2 cell effector function (Trompette et al., 2014).
They found that the microbial community structure changed with age and allergy development and interestingly that the alterations in the intestinal microbiota from young to old mice resembled the microbial structure of mice after house dust mite challenge. These findings suggest that the commensal microbiota maintain host defenses to infectious agents by facilitating a normal inflammatory response to pulmonary pathogens. During normal homeostasis all three components interact normally, which facilitates intestinal crosstalk with extra-intestinal tissues.
Therefore, it is conceivable that differences in microbiota composition may also affect oral tolerance.
The changes in the intestinal microbial communities were also associated with increased levels of serum IL-17A.
However, in critically ill patients, loss of the balance between these highly interrelated systems results in the development of systemic manifestations of disease, specifically SIRS, ARDS, or MODS (Clark and Coopersmith, 2007).
The mechanisms governing gut-derived sepsis and ARDS are poorly understood and are actively being investigated.
Vital and colleagues also suggest the composition of the gut microbiota changes with pulmonary allergy, indicating bidirectional gut-lung communications (Vital et al., 2015).



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