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Bacteria Causing Gastrointestinal Infections
Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019
B. Vinoth, M. Krishna Raja, B. Agieshkumar
B. fragilis are anaerobic commensal bacteria found in human intestine. Only during 1980s, it was found to be associated with diarrheal illness in humans. They produce an enterotoxin called B. fragilis enterotoxin (BFT), also called as fragilysin, which causes secretion of IL-8 and leads to inflammation. They also cause increased intestinal permeability. The usual clinical feature is development of nonbloody diarrhea in children and adults. It is diagnosed by selective culture under anaerobic condition. Genetic and biological assays are required to diagnose the presence of the enterotoxin and are not routinely available. Because the diagnosis is rarely done, the exact role of antibiotics is not clearly known.
Bacteroides
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Besides capsule, others factors associated with the virulence in Bacteroides spp. include an enterotoxin called fragilysin. Enterotoxigenic B. fragilis (ETBF) is implicated in inflammatory intestinal diseases,5–7 and the intestinal colonization can produce acute or chronic intestinal inflammation. This toxin alters the F-actin structure causing disruption of the epithelial barrier producing diarrhea.8,9
Gut Bacteroides species in health and disease
Published in Gut Microbes, 2021
Bfr can be classified into two subtypes based on their pathogenic potential 1) non-enterotoxigenic strains that do not encode the Bfr toxin, and 2) enterotoxigenic Bfr strains that do have the bft genes that encode the toxin.92 Toxigenic strains of Bfr have been associated with different disease conditions of the human gut, including ulcerative colitis, toxin-mediated acute diarrhea, and bacteremia.93,94 The Bfr toxin (fragilysin) is one of the best-researched virulence factors among Bacteroides spp. It exists in three isoforms, BFT 1–3, with BFT-2 having the greatest potential to elicit tissue damage. Among isolates from humans, BFT-1 is the most common toxin variant, while the BFT-3 has a geographical propensity for Southeast Asia.95,96 As a heat-labile nickel ion-dependent metalloprotease, it shares substantial similarity with the tetanus and botulinum toxins. BFT is produced as a pre-protein and is cleaved by the fragipain cysteine protease to form the mature 20 kDa secreted toxin that is enterotoxic and cytotoxic in lamb ileal loop assays and HT29 cell lines.97
“Driver-passenger” bacteria and their metabolites in the pathogenesis of colorectal cancer
Published in Gut Microbes, 2021
Marion Avril, R. William DePaolo
Bacteroides fragilis is a common gram-negative anaerobic bacterium belonging to the Bacteroidetes phylum. B. fragilis has two subgroups, the enterotoxigenic strains (ETBF) that possess the bft gene encoding the B. fragilis toxin (BFT or fragilysin), while the nontoxigenic strains (NTBF) do not. ETBF has been implicated in diarrhea41 and is considered oncogenic under certain circumstances due the actions of BFT which can induce DNA damage and inflammation in vivo.18,42 BFT is a metalloproteinase and has been shown to rapidly alter the structure and function of colonic epithelial cells, including the cleavage of the tumor suppressor protein, E-cadherin. Once cleaved this triggers β-catenin/Wnt signaling leading to permeability of the intestinal barrier. One of the molecular mechanisms in which ETBF triggers colitis and induces colon tumorigenesis in multiple intestinal neoplasia (Min) mice, is via the activation of signal transducer and activator of transcription 3 (STAT3) and induction of T-helper type-17 (TH17) T cell responses.
Role of microbiota and related metabolites in gastrointestinal tract barrier function in NAFLD
Published in Tissue Barriers, 2021
Maria Victoria Fernandez-Cantos, Diego Garcia-Morena, Valeria Iannone, Hani El-Nezami, Marjukka Kolehmainen, Oscar P. Kuipers
As previously discussed, E-cadherin is a crucial AJ for intercellular associations, and its loss of function has been linked to several pathological processes. In fact, deletion of E-cadherin in mice resulted in severe weight reduction, loss of intestinal epithelial architecture and problems in the differentiation of secretory cell lineages.118 In particular, Paneth cell maturation and placement along the intestine is affected by the loss of E-cadherin. The reduction in Paneth cell count impairs proper bacterial defense, facilitating the approach of pathobionts to the IECs. Interestingly, the enterotoxin fragilysin, produced by Bacteroides fragilis, can interact and cleave the extracellular domains of E-cadherin,119 resulting in intestinal permeability. Bacteroides is a common resident in the gut and conflictive results are reported when assessing its contribution to liver disease (Supplementary Table 1). This bacterium, typically considered a commensal, has also been found to be responsible for a significant increase in the biofilm mass in patients with Crohn’s disease.120 However, the apparent pathological relation with Crohn’s disease is as well challenged by Hsiao et al.121 Treatment of the model maternal immune activation (MIA) mice with B. fragilis rendered an improvement in gut barrier integrity and promoted the restoration of the relative abundance of 6 operational taxonomic units in the absence of B. fragilis colonization. Remarkably, treatment with B. fragilis was able to correct autism spectrum disorder-related behavioral abnormalities in this mice model.121 This highlights how members of the same genus or family contribute differently to the homeostasis of the intestine, blurring their role in health and in disease. How members of the same species account for different effects, possibly depending on the environmental cues (such as diet, or genetic background); as well as, how strain-level identification of the BGM is needed to account for strain-specific traits, are important outstanding questions.