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Commensal microbiota and its relationship to homeostasis and disease
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Jonathan Braun, Elaine Y. Hsiao, Nicholas Powell
Sequencing of 16S ribosomal RNA genes confirmed differences in the intestinal microbiota community profile between Jackson Laboratories and Taconic Farms mice. In particular, a bacterium from the genus Arthromitus, termed segmented filamentous bacterium (SFB), was present in Taconic mice but not in Jackson mice (Figure 19.4). This is the same organism that was shown many years ago to restore systemic and mucosal immunity when monocolonized into germ-free mice. SFB could be transmitted to Jackson mice if they were cohoused in the same cages as Taconic mice, which also resulted in successful acquisition of mucosal TH17 responses in Jackson mice. Critically, monoassociation of germ-free mice with SFB alone reinstated mucosal TH17 cells. The TH17-promoting property of SFB appears to be relatively selective because other T-cell lineages are less dramatically affected. SFB also reduced intestinal regulatory T cells, favoring a more inflammatory bias in gut-resident T cells.
The Etiology of the Antiphospholipid Syndrome
Published in Howard J.A. Carp, Recurrent Pregnancy Loss, 2020
Sara De Carolis, Giuseppina Monteleone, Cristina Garufi, Rotem Inbar, Miri Blank, Yehuda Shoenfeld
Alteration of microbiome “dysbiosis” can induce antiphospholipid syndrome in people with genetic predispositions [14]. Segmented filamentous bacteria (SFB) influence T cells-phenotype, T-dependent, and T-independent antibody production [15]. If homeostasis is disrupted (by infections or drugs), proinflammatory interactions could occur with local and systemic effects on the immune system. These effects include breaches of the mucosal barriers and generation of commensal specific memory T cells and autoantibodies. Therefore, commensal bacteria may promote breaks in tolerance and the induction of persistent aPL in predisposed individuals. Roseburia intestinalis, which is prevalent in the intestine of APS patients, has many homologous sequences to both the major B and T cell epitopes and thus could stimulate lymphocytes [14].
The Microbiome – Role in Personalized Medicine
Published in David Perlmutter, The Microbiome and the Brain, 2019
In the intestinal mucosa, Th17 cells impart important immune-modulating effects. It has been found that the adherence of specific segmented filamentous bacteria to the gut epithelium results in the induction of Th17 producing cells.40 Th17 cells provide protective immunity to fungi and extracellular bacterial infections and appear to have a role in protecting against gastric cancer, but are also involved in chronic inflammation. These cells produce IL-17, a cytokine that is associated with autoimmunity.41 Th17 cells can remain dormant for long periods of time and may only be activated and become contributors to inflammation as a result of dysbiosis or exposure to a triggering agent. This example once again illustrates the importance of a complex, stable gut microbial ecosystem in establishing and maintaining the balance between pro and anti-inflammatory immunomodulatory effects.
Gut microbiome in type 1 diabetes: the immunological perspective
Published in Expert Review of Clinical Immunology, 2023
Elena Rampanelli, Max Nieuwdorp
In another report, Kriegel et al. studied the variation in intestinal colonization by segmented filamentous bacteria (SFB) in the NOD strain, discovering a connection between SFB colonization and disease penetrance in female NOD mice. In fact, the authors report a clear-cut segregation of high incidence with SFB negativity as 91% of female NOD mice lacking intestinal SFB develop T1D by 30 weeks of age, whereas solely 16% of SFB colonized mice display diabetes within 30 weeks. SFB-positivity was associated with a Th17 signature and expansion of Th17 CD4 T cells in the small intestinal lamina propria, but did not affect other T cell subtypes [102]. As the pathogenic role of Th17 in T1D is controversial, an attractive explanation of the protective function of intestinal Th17 cell is that the marked increase in the Th17 compartment can lead to the inhibition of islet-reactive Th1 cells. This hypothesis is supported by the reported Th17-mediated suppression of Th1 cells in a colitis murine model [103].
Visualizing germination of microbiota endospores in the mammalian gut
Published in Gut Microbes, 2022
Ningning Xu, Liyuan Lin, Yahui Du, Huibin Lin, Jia Song, Chaoyong Yang, Wei Wang
Of special note, as a heavily studied spore-forming bacterial species, segmented filamentous bacteria (SFB) play important roles in inducing T helper cell 17, and many other immunity-related effects.31,32 In the mammalian gut, SFB normally attach to the ileal epithelium, extend from its distal end and release endospores from the maturing filaments,33 which facilitates its vertical transmission from parents to offspring and horizontal transmission between hosts.34,35 Two intracellular offsprings formed within a differentiating filament can be released into the intestines and function as endospores.34 Intriguingly, here we observed an intersegmental SFB germinating in the gut (Figure 5(g)), the labeling pattern of which was very different from these observed in other gut bacteria (Figure 5(f)). The Cy5ADA-labeled segments were probably owing to several pairs of intracellular offsprings that germinated within their mother cells. It was also possible that these cells already underwent one cell division, considering their uniform labeling signals on the cell walls and the fact that no traces of their mother cells could be observed. The life-cycle of SFB has been investigated mostly by scanning electron microscopy analysis of the mammalian intestine samples.33 Our labeling strategy provides a unique perspective to study their activities and transmission in the gut.
Auto-reactivity against gut bacterial peptides in patients with late-onset diabetes
Published in Autoimmunity, 2020
Mohammad Sajid, Krishna Biswas, Harpreet Singh, Sapna Negi
Gut bacteria harbours several metabolic genes and therefore, immunity against these gut bacterial proteins may be harmful and may contribute to late-onset diabetes. The gut microbes have shown their role in the progression of various autoimmune diseases like systemic lupus erythematosus, multiple sclerosis, rheumatoid arthritis (RA), psoriasis, type-1 diabetes (T1D), and T2D [5–11]. The composition of gut microbes induces the upregulation of Th17 lymphocytes and can produce cytokine IL-17. Increased production of IL-17 can induce autoimmune responses [12]. This was also demonstrated by inhabiting segmented filamentous bacteria (SFB) in germ-free mice (GF), which gave rise to auto-antibodies and stimulated Th17 cells in lamina propria of the gut [13]. In addition, the commensal gut microbe showed similarity with myelin oligodendrocyte glycoprotein of the host and induction of complex spontaneous demyelinating autoimmune disease [14]. Further, gut microbe’s proteins have a resemblance with self-antigens of pancreatic tissue. For instance, a protein (Mgt) of Leptotrichia goodfellowii exhibit likeness with pancreatic islet located glucose-6-phosphatase related protein (IGRP). A study on transgenic non-obese diabetic mice demonstrated the presence of IGRP-specific cytotoxic T lymphocytes strongly promote T1D development through the gut microbiota [15].