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Gefilus® products contain the best-known and world’s most studied lactic acid bacteria, Lactobacillus rhamnosus GG. January 23, 2013 Leave a Comment Probiotics are micro-organisms that are a good form of bacteria.
Thus, they improve the intestinal function and are effective in treating a number of ailments. Probiotics promote a strong immune system and regulate healthy immune response as certain probiotic bacteria improve some components of the immune response. They reinforce the immunity of the intestinal mucus membrane, potentially change and improve immune cells, and strengthen the bacteria already present in your gut.
Probiotics are highly beneficial when dealing with a gastrointestinal problem called antibiotic-associated diarrhea.
Consuming probiotics while taking a course of antibiotics restores the good bacteria that are killed by the antibiotic. Besides, individuals who are prone to stomach or bowel infections and travelers’ diarrhea should take probiotics. Before administering this treatment on your baby, though, make sure you consult with your doctor about it. It relieves symptoms such as stuffy nose and sore throat that are caused due to immune system’s reaction to the virus that causes common cold.
Probiotics, especially strains like Bifidobacterium infantis and Lactobacillus plantarum improve the symptoms of Irritable Bowel Syndrome (IBS) in women. Plus, they are popularly used to prevent and cure Candidiasis yeast infection and vaginal bacterial infections, which are quite common in women. They tend to influence the way in which bile acids are metabolized, thereby altering the amount of fats the body absorbs.
Foods that are rich in unpasteurized probiotics include plain unflavored yogurt, kefir, tempeh, miso (tofu and vegetable broth soup), sauerkraut (made from fermented cabbage), kimchi, kombucha tea, and pickles. Microbial Ecology, Nutrition & Health Research Group, Institute of Agrochemistry and Food Technology, National Research Council (IATA-CSIC), Avda. It is widely recognized that the intestinal microbiota plays a role in the initiation and perpetuation of intestinal inflammation in numerous chronic conditions. Effects of Lactobacillus GG have been proven in over 700 scientific studies, over 190 of them are clinical studies. Lactobacillus rhamnosus or LGG, in particular, is known to relieve viral or antibiotic induced diarrhea.
Probiotics minimize lactose intolerance, too, because they contain lactic acid bacteria, which convert the lactose into lactic acid. In addition, researchers have found that probiotics may also help fight abdominal obesity and prevent obesity-related disorders (like type-2 diabetes).
Besides, you can take probiotic supplements containing Lactobacillus acidophilus, Lactobacillus casei, Streptococcus thermophilus, and Bifidobacteria bifidum. Glownym skladnikiem preparatu sa bakterie szczepu Lactobacillus rhamnosus GG, ktory pomaga przywrocic rownowage mikroflory jelitowej. Jest zbiorem wielu przydatnych informacji o ciazy oraz macierzynstwie, ktore nie moga byc traktowane jako zalecenia, ale wylacznie jako pomoc w poznawaniu tajnikow ciazy, wychowania i pielegnacji dzieci.
Most studies report intestinal dysbiosis in celiac disease (CD) patients, untreated and treated with a gluten-free diet (GFD), compared to healthy controls.
IntroductionCeliac disease (CD) is a chronic immune-mediated inflammatory disease affecting the small bowel, triggered by gluten ingestion in genetically susceptible individuals.
Specific host genetic makeup and environmental factors could promote the colonization of pathobionts and reduce symbionts, thus leading to dysbiosis.
Host Genetics and Intestinal MicrobiotaAlthough gut microbiota composition shows large inter-individual variability, family members have more similar microbiota than unrelated individuals and, indeed, the same bacterial strains are shared among family members [47,48,49]. Zaistniale problemy czy watpliwosci dotyczace konkretnych przypadkow nalezy bezzwlocznie konsultowac z prowadzacym lekarzem ginekologiem lub innym stosownym specjalista w danej dziedzinie. CD patients with gastrointestinal symptoms are also known to have a different microbiota compared to patients with dermatitis herpetiformis and controls, suggesting that the microbiota is involved in disease manifestation. Even though CD is an infra-diagnosed disorder, it is currently considered the most common food intolerance, affecting approximately 1% of European ancestry individuals.CD is a complex multifactorial disorder involving both genetic and environmental factors.
Dysbiosis may contribute to disrupting the immune homeostasis and gut integrity, thereby favoring CD onset and aggravating the pathogenesis. These similarities between the microbiota of related members most likely reflect the influence of the host genetic makeup although the shared environmental factors have also been shown to have an effect. Furthermore, a dysbiotic microbiota seems to be associated with persistent gastrointestinal symptoms in treated CD patients, suggesting its pathogenic implication in these particular cases. Over 30 years ago, a study reported that the fecal microbiota of monozygotic human twins was much more similar than that of dizygotic twins [47].Some years ago, researchers tested whether specific taxa co-segregated as quantitative traits linked to genetic markers using quantitative trait loci (QTL) analysis in mice [50].

GFD per se influences gut microbiota composition, and thus constitutes an inevitable confounding factor in studies conducted in CD patients. The QTL detection approach revealed 18 host-associated QTLs having a linkage with the abundance of 26 specific microbial taxa. To improve our understanding of whether intestinal dysbiosis is the cause or consequence of disease, prospective studies in healthy infants at family risk of CD are underway. With the introduction of GWAS (genome wide association studies) and the Immunochip study, an additional 39 non-HLA regions of susceptibility have been associated with CD development, some of which are shared with other autoimmune diseases [2,3,4,5,6,7].
In addition, they established that one QTL is often associated with more than one taxon, indicating that human genetics may strongly influence the microbiota community structure. Komandytowa nie odpowiada za tresc reklam, nie ponosi rowniez zadnych konsekwencji prawnych ani odpowiedzialnosci za nastepstwa mogace wyniknac na skutek zastosowania podanych informacji bez wczesniejszej konsultacji z lekarzem.
CD is a complex immune-related disorder with the best characterized genetic component; however, only an approximate 31% of its heritability has been explained so far, suggesting that other genetic factors besides gene–gene and gene–environment interactions might be involved in disease development [1]. Not surprisingly, most of the genes that have been identified as genes associated with microbiota changes encode factors involved in bacterial sensing and immune reactions, while some others are involved in metabolism [52]. Studies have also revealed an altered expression of non-specific CD risk-genes involved in host–microbiota interactions in the intestinal mucosa of CD patients, such as those of Toll-like receptors (TLRs) and their regulators [8]. The first human gene for which variation was shown to influence the gut microbiota was Mediterranean fever (MEFV) [51]. Furthermore, 81% of CD associated genetic variants are located in noncoding regions of the genome [9], suggesting that one of the main mechanisms by which genetic variation could have an impact on CD is by affecting the gene expression levels.
Specifically, this study revealed that changes in the human gut microbiota are associated with a single mutation in MEFV, which leads to a hereditary autoinflammatory disorder affecting people with Mediterranean ancestors, the so-called familial Mediterranean fever.PRRs as well as antimicrobial peptides are key factors controlling the intestinal microbiota composition. We also summarize the current knowledge about the potential mechanisms of action of the intestinal microbiota and specific components that affect CD pathogenesis.
Thus, the altered expression of CD-risk genes, as well as other non-specific CD genes triggered by genetic and epigenetic factors, may contribute to disturbing the host–microbiota interaction, and shift immune balance in CD subjects. Indeed, deficiencies in these genes lead to changes in the composition of the gut microbiota [52].
Similar findings have been reported for inflammatory bowel disease (IBD) [10], a disorder characterized by a deregulated immune response against the microbiota, triggered by specific genetic determinants [11].CD commonly appears in early childhood after the first exposures to dietary gluten, which is its main environmental trigger.
Animal studies have indicated that genes coding for inflammasome-related proteins, which are also involved in the recognition of microbial or other damage signals, influence intestinal microbiota composition and colitis development. However, there are increasing numbers of subjects experiencing CD onset in early and late adulthood [12], which suggests that additional environmental factors must play a role in CD development. Actually, deficient mice in the pyrin 6 member of the nucleotide-binding oligomerization domain-like receptor (Nlrp6) showed different fecal microbiota characterized by increased representation of Bacteroidetes (Prevotellaceae) and TM7, reduced IL-18 production by epithelial cells and exacerbation of colitis induced by exposure to dextran sodium sulfate [53].
In fact, other environmental factors that influence the early gut microbiota composition such as birth delivery mode and milk-feeding type, intestinal infections and antibiotic intake, have also been associated with the risk of developing CD [13,14,15,16,17,18]. Very recently, a study has reported that NLRP6 inflammasome regulates goblet cell mucus secretion, showing that NLRP6 inflammasome-deficient mice are highly susceptible to persistent infection since they are unable to clear enteric pathogens from the mucosal surface [54]. Thus, a number of epidemiological studies indicate that several perinatal factors participate in conjunction to modulate CD risk.Many complex immune-mediated diseases have been linked to changes in the composition of the gut microbiota and its genome (microbiome), including CD [19,20,21,22,23]. Some years ago, the capacity of interferon (IFN) signaling pathways to modulate the microbiota composition was demonstrated in mice [55]. It has also recently been observed that the microbiota differs among the different subgroups of CD patients stratified according to specific clinical manifestations [24]. Moreover, although the vast majority of patients diagnosed with CD respond to a GFD there is a subgroup of CD patients that do not show clinical improvement after adherence to a GFD [24]. In particular, patients suffering persistent symptoms on a long-term GFD also show an altered microbiota composition [25]. Interestingly, several of these genes have been shown to have a role in shaping the microbiota.
CD14 is, together with TLR-4, involved in the recognition and signal transduction of bacterial endotoxin or lipopolysaccharide, a major component of the bacterial cell wall of Gram-negative bacteria.
Particularly, many of the IBD-susceptibility genes regulate host–microbial interactions [57].
Some of these loci are involved in bacterial sensing and immune reactions and might contribute to explaining the relationship between IBD and intestinal dysbiosis. Soluble CD14 (sCD14) is commonly used as an indicator of innate immunity cell activation in response to mucosal translocation of Gram-negative bacteria or their components [26]. For instance, nucleotide-binding oligomerization domain containing 2 (NOD2) is an intracellular sensor of bacterial peptidoglycan strongly expressed in Paneth cells, regulating their function, which is to release granules containing antimicrobial peptides in response to bacteria [58].
Interestingly, it has recently been reported that sCD14 protein seropositivity is increased in untreated CD patients [27]. NOD2 has been identified as a susceptibility gene for Crohn’s disease and different NOD2 polymorphisms have been associated with loss-of-function of the protein.

These increased sCD14 serum levels in CD could be the consequence of translocation of commensal intestinal bacteria, which could aggravate CD pathogenesis. Recently, a study focusing on IBD revealed a significant association between NOD2 risk allele counts and increased relative abundance of Enterobacteriaceae [59]. Taken together, all this evidence suggests a role for the microbiota in disease manifestation, pathogenesis and risk.
Furthermore, NOD2-deficient mice display a diminished ability to kill bacteria and increased loads of commensal bacteria, demonstrating that NOD2 is essential for regulating intestinal microbiota [60]. Subsequent studies have demonstrated that NOD2 genotypes also affect human microbial composition [61].
We also summarize the current understanding of the potential mechanisms of action of the intestinal microbiota and its specific components in CD pathogenesis. NOD2-deficient mice displayed increased responses to TLR stimulation, which might mirror the situation in genetically susceptible individuals [62].
Therefore, it is tempting to speculate that NOD2 polymorphisms could increase susceptibility to Crohn’s disease by suppressing TLR homeostasis, which would trigger a pathogenic response to the commensal microbiota. A recent study focusing on IBD demonstrated reproducible effects of a number of host genes on the microbiome taxonomic structure across two or more cohorts; some of the studied genes have known involvement in microbial handling while others are of unknown function [59].
Interestingly, beside NOD2, tumor necrosis factor (ligand) superfamily member 15 (TNFSF15) and subunit beta of interleukin 12 (IL12B) showed significantly conserved directionality effects on bacterial taxa between at least one pair of studies. A functional enrichment analysis showed that genes regulating the innate immune response, the JAK-STAT pathway and other immunity-related pathways, seem to be related with microbiome features [59]. Most likely some of those genotype-microbiome associations may be IBD-independent and relevant to individuals with other diseases such as CD.Another study described that the ?-1, 4-n-acetyl-galactosaminyltransferase 2 (B4galnt2) gene, encoding a mucosal surface glycan with an important role in host–microbiota interaction, influences the abundance of specific bacterial taxa microbiota composition [63]. A recent study reported the link between Cystic fibrosis transmembrane conductance regulator (CFTR) gene variants and shifts in fecal microbiota [64].
Furthermore, a rare polymorphism located within the immunity-related GTPase family M (IRGM) gene (involved in autophagy and with a potential role in microbiota homeostasis) is reported to show a significant correlation with a Prevotella-predominant enterotype [65].Another recent study has compared the microbiota of 416 twin pairs, identifying many specific members of the gut microbiota whose abundances were influenced by the host genetic makeup, while other members seem to be determined by environmental factors [44].
Specifically, the family Christensenellaceae showed the highest heritability, forming a co-occurrence network with other heritable bacteria and Archaea in lean individuals; however, Bacteroidetes seem to be mostly determined by the environment. Interestingly, the study showed that Christensenellaceae was enriched in lean individuals, and was associated with reduced weight gain in mice.
Therefore, the results indicate that host genetics influence gut microbiome composition, and may do so in ways that impact host metabolism [44]. A variety of evidence suggests that a substantial number of genetic factors in humans may contribute with a relatively weak effect on the microbiota composition. Future studies should focus on analyzing all the host alleles underlying heritability of the gut microbiome as this would shed more light on the relationship between host genotype and microbiome composition.
Epigenetics and Intestinal Microbiota: A New Emerging FieldNowadays, it is well established that there are changes in gene expression or cellular phenotype triggered by epigenetic modifications, such as methylation or non-coding RNAs (ncRNAs), defined as RNA molecules transcribed from DNA but not translated into proteins. These are involved in post-transcriptional regulation of gene expression, among others, and not caused by changes in the DNA sequence.
Interestingly, blood DNA methylation patterns are associated with gut microbiota profiles [80] and a recent study has also indicated the relationship between microbiota and methylation level of the free fatty acid receptor 3 gene, involved in metabolism and the inflammatory response [81].
Furthermore, methylation level at the IFNG locus is correlated with the immune response to microbial components and with the expression of IFN-? in ulcerative colitis patients [82]. Until now, different studies have reported a link between miRNAs, a group of small ncRNAs, and microbiota [83]. They showed nine miRNAs differentially expressed in the ileum and colon of colonized mice compared to germ-free mice [84]. Moreover, authors found that 34 putative miRNA target genes encode for proteins involved in the regulation of the intestinal barrier function and immune response, indicating the interplay between microbiota and caecal miRNA signature [85].
Modifications of histone acetylation, related to local relaxation of the chromatin and access for transcription machinery by histone deacetylase (HDACs) are also critical in epigenomic regulation.
HDACs are inhibited by commensal bacterial-derived SCFAs in innate and adaptive immune cell populations, suggesting that the metabolic activity of commensal bacterial can modify the epigenome of host cells and in turn alter their development and function [86]. In fact, SCFAs derived from commensal bacteria exert anti-inflammatory effects in the colon, partially by stimulating histone acetylation of Forkhead box P3 (FoxP3) locus in naive CD4+ T cells and, thereby increasing FoxP3 expression and promoting the differentiation of Tregs [87]. However, research into the role of epigenetics in regulating the cross talk between the host and the microbiota is in the early stages, while studies related to CD have yet to be undertaken. Intestinal Dysbiosis and Its Potential Pathogenic Role in CDMost observational studies in children and adults with CD have shown alterations in the intestinal microbiota composition compared to control subjects [21,22,101,102]. In this context, we performed studies using different quantitative methods to assess microbiota composition, such as fluorescence in situ hybridization (FISH) and quantitative PCR.

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