Bacteroides fragilis plays an important physiological role in the adult colon. Bacteroides is a Gram-negative, non-spore forming, obligate anaerobic bacteria normally found in the human intestines, mouth, upper respiratory tract, and genital tract. Bacteroides expresses polysaccharide A, which can induce regulatory T cell growth and cytokine expression that are protective against colitis.
There are 160 major bacteria among the 1,000 to 1,150 species of bacteria which colonize the human intestinal tract. Two dominant microflora in the human distal gut, Bacteroides and Firmicutes phyla, account for 90% of the bacterial flora.
Inflammatory bowel diseases:
Many studies have related Bacteroides to the development of IBD. Inflammatory bowel disease (IBD) which includes Crohn’s disease (CD), ulcerative colitis (UC), and indeterminate colitis (IC) is a chronic relapsing inflammatory disorder of the gastrointestinal tract of unclear etiology. One hypothesis is that the inflammation results from altered microbiota in a genetically susceptible host. Intestinal flora in healthy individuals can demonstrate significant variety. As individuals age, their intestinal microbial flora tend to become more similar. There is a healthy balance of microflora in the gastrointestinal tract in normal individuals. This balance is disrupted in disease.
Possible treatment options:
Several lines of evidence support the notion that gut dysbiosis contributes to the pathogenesis of IBD. Beneficial bacteria are less abundant while pathogenic bacteria are increased in IBD patients. This imbalance of the gut microbiota is not merely a secondary consequence of disease. Rather, it is thought that a dysbiotic microbiota has inflammatory potential and/or interfere with protective/regulatory function of the immune system. Hence, novel therapeutic strategies that selectively target dysbiosis have attracted considerable interest and offer hope for more effective IBD treatment options.
For instance, fecal microbiota transplantation (FMT), which aims to restore normal gut microbial composition and function appears to be an effective treatment for IBD. It has been shown that FMT can be effective for the treatment of CDI in IBD patients, resulting in the normalization of altered microbial composition and metabolic function, and elimination of C. difficile. Indeed, microbial diversity and richness in IBD patients treated with FMT increase and become similar to those of healthy donors. Additionally, FMT restores secondary bile acid metabolism in the intestine and ameliorates gut damage. Thus, FMT seems to be a promising therapeutic approach that restores/enhances microbiota-mediated resistance to pathogens.
Likewise, dietary intervention is another approach used to restore normal microbial composition and function, as it has been reported that diet is a powerful driver of microbial structure in the gut. Elemental diet has been used in the treatment of IBD, in particular to manage the symptoms of CD. Cohort studies have shown that elemental diet has an impact on the composition of the gut microbiota, and induces mucosal healing and clinical remission of CD. Mounting evidence suggests that a diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) can effectively reduce GI symptoms in patients with irritable bowel syndrome by altering microbial composition and luminal metabolism. In this context, pilot studies have demonstrated that a low-FODMAPs diet can significantly ameliorate gut dysfunction in some IBD patients.
References:
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5599888/
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5143693/
- https://www.gastrojournal.org/article/S0016-5085(06)00015-1/fulltext
- https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD007350.pub2/abstract
- https://insights.ovid.com/crossref?an=00000434-201210000-00002
- https://science.sciencemag.org/content/308/5728/1635
- https://www.nature.com/articles/nrmicro1978
- https://mic.microbiologyresearch.org/content/journal/micro/10.1099/mic.0.038588-0
- https://science.sciencemag.org/content/332/6032/974
- https://www.sciencedirect.com/science/article/pii/S1743919110000403?via%3Dihub
- https://link.springer.com/article/10.1023%2FB%3ADDAS.0000042241.13489.88
- https://www.tandfonline.com/doi/abs/10.1080/003655202320378220
A lower level of Bacteroides was demonstrated in Crohn’s disease and ulcerative colitis patients, especially CD and UC patients with active disease. UC patients in remission also had a lower level of Bacteroides than controls. Patients with active UC had lower Bacteroides levels than patients in remission.
Mild signs and symptoms can often be controlled by managing stress and by making changes in your diet and lifestyle.
Try to:
- Avoid foods that trigger your symptoms
- Eat high-fiber foods
- Drink plenty of fluids
- Exercise regularly
- Get enough sleep
Your doctor might suggest that you eliminate from your diet:
- High-gas foods. If you experience bloating or gas, you might avoid items such as carbonated and alcoholic beverages, caffeine, raw fruit, and certain vegetables, such as cabbage, broccoli and cauliflower.
- Gluten. Research shows that some people with IBS report improvement in diarrhea symptoms if they stop eating gluten (wheat, barley and rye) even if they don't have celiac disease.
- FODMAPs. Some people are sensitive to certain carbohydrates such as fructose, fructans, lactose and others, known as FODMAPs — fermentable oligo-, di-, and monosaccharides and polyols. FODMAPs are found in certain grains, vegetables, fruits and dairy products. Your IBS symptoms might ease if you follow a strict low-FODMAP diet and then reintroduce foods one at a time.
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Gram-negative species of the Bacteroidetes phylum. Immune-modulating normal gut species. Believed to be involved in microbial balance, barrier integrity, and neuroimmune health.
High levels may result from reduced digestive capacity or constipation.
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A2142C, A2142G, A2143G, A926G, Adenovirus 40/41, AGA926-928TTC, Akkermansia muciniphila, Amoxicillin, Ancylostoma duodenale, Anti-gliadin IgA, Ascaris lumbricoides, b-Glucuronidase, Bacillus spp., Bacteroides fragilis, Bacteroidetes, Bifidobacterium spp., Blastocystis hominis, C. difficile, Toxin A, C. difficile, Toxin B, Calprotectin, Campylobacter, Candida albicans, Candida spp., Chilomastix mesnili, Citrobacter freundii, Citrobacter spp., Clarithromycin, Clostridia (class), Cryptosporidium, Cyclospora spp., Cytomegalovirus, Desulfovibrio spp., Dientamoeba fragilis, E. coli O157, Elastase-1, Endolimax nana, Entamoeba coli, Entamoeba histolytica, Enterobacter spp., Enterococcus faecalis, Enterococcus faecium, Enterococcus spp., Enterohemorrhagic E. coli (EHEC), Enteroinvasive E. coli/Shigella, Enterotoxigenic E. coli LT/ST, Eosinophil Activation Protein (EDN/EPX), Epstein-Barr Virus, Escherichia spp., Faecalibacterium prausnitzii, Firmicutes, Firmicutes:Bacteroidetes Ratio, Fluoroquinolones, Fusobacterium spp., Geotrichum spp., Giardia, gyrA D91G, gyrA D91N, gyrA N87K, gyrB R484K, gyrB S479N, Helicobacter pylori, Klebsiella pneumoniae, Klebsiella spp., Lactobacillus spp., M. avium subsp. paratuberculosis, Methanobacteriaceae (family), Microsporidium spp., Morganella spp., Necator americanus, Norovirus GI/II, Occult Blood - FIT, PBP1A N562Y, PBP1A S414R, PBP1A T556S, Pentatrichomonas hominis, Prevotella spp., Proteus mirabilis, Proteus spp., Pseudomonas aeruginosa, Pseudomonas spp., Rhodotorula spp., Rodotorula spp., Roseburia spp., Salmonella, Secretory IgA, Shiga-like Toxin E. coli stx1, Shiga-like Toxin E. coli stx2, Staphylococcus aureus, Staphylococcus spp., Steatocrit, Streptococcus spp., Taenia spp., Tetracycline, Trichuris trichiura, Vibrio cholerae, Virulence Factor, babA, Virulence Factor, cagA, Virulence Factor, dupA, Virulence Factor, iceA, Virulence Factor, oipA, Virulence Factor, vacA, Virulence Factor, virB, Virulence Factor, virD, Yersinia enterocolitica, Zonulin