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T lymphocyte populations within the lamina propria
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Thomas T. MacDonald, Antonio Di Sabatino
Further support for the idea that specific types of bacteria can induce markedly different types of T-cell responses comes from the observations that mice from different suppliers have markedly different numbers of TH17 cells in their small intestine, despite having identical numbers of T cells in their gut. It was shown that adult germ-free mice had virtually no TH17 cells in their gut; however, on colonization with a microbial flora, TH17 cells became abundant. If adult normal mice were treated with antibiotics to lower the flora, then TH17 cell numbers were reduced by 50%. When mice from different vendors were examined, most had abundant TH17 cells in their intestine, apart from mice from the Jackson Laboratory, in which there were essentially none. Likewise, reconstitution of germ-free mice with the altered Schaedler flora, for many years considered to be the gold-standard specific pathogen free (SPF) flora, also did not result in mucosal TH17 cells. Detailed analysis of the components of the microflora in mice from different vendors showed that the key organism that drives TH17 responses was an unculturable segmented filamentous bacterium (SFB) related to clostridia. Mice harboring SFB are somewhat more resistant to C. rodentium infection than mice lacking SFB.
16S rRNA sequencing analysis: the devil is in the details
Published in Gut Microbes, 2020
Amy M. Tsou, Scott W. Olesen, Eric J. Alm, Scott B. Snapper
Helicobacter species play a complex role in human health: H. pylori causes peptic ulcers and gastric cancers but reduces the risk of inflammatory bowel disease (IBD), while enterohepatic Helicobacter species confer an increased risk of IBD.1 To explore the effect that Helicobacter species have on other members of the gut microbiota, we colonized one group of mice with a standardized gut community (altered Schaedler flora, ASF) and another group of mice with the ASF community and also Helicobacter bilis.2–4 We performed paired-end 16S sequencing on stool collected from the two groups of mice. We separately denoised forward, reverse, and merged reads with Deblur.5 Finally, we compared closed- and open-reference calling in two popular bioinformatic pipelines, Qiime 1 and Qiime 2.6,7
Validation studies for germ-free Smad3-/- mice as a bio-assay to test the causative role of fecal microbiomes in IBD
Published in Gut Microbes, 2020
Jisun Paik, Stacey Meeker, Charlie C. Hsu, Audrey Seamons, Olesya Pershutkina, Jessica M. Snyder, Thea Brabb, Lillian Maggio-Price
Though our studies employ H. bilis as a trigger of IBD in the SPF donor mice, our mono-colonization experiments suggested that H. bilis on its own is not likely the cause of IBD in GF recipient mice; H. bilis alone only induced mild to moderate inflammation in the cecum that quickly resolved. Our results are similar to those reported by Dieleman et al. in that mono-colonization with another Helicobacter, H. hepaticus, does not cause IBD in GF Il10-/- mice at 9 and 12 weeks following colonization.27 In addition, H. bilis was reported to promote more severe gut inflammation in wild type mice (C3H/HeN and C57BL/6) colonized with Altered Schaedler Flora compared to H. bilis mono-colonized mice when they were treated with a low dose of dextran sodium sulfate, a chemical trigger of IBD.28 Our data and these previous studies demonstrate that other enteric bacteria are needed to induce severe intestinal inflammation upon Helicobacter infection.4,12,29
Bacterial imbalance and gut pathologies: Association and contribution of E. coli in inflammatory bowel disease
Published in Critical Reviews in Clinical Laboratory Sciences, 2019
Shahanavaj Khan, Ahamad Imran, Abdul Malik, Anis Ahmad Chaudhary, Abdur Rub, Arif Tasleem Jan, Jakeera Begum Syed, Christian Rolfo
The delicate balance between TH17/TH1 effector cells and TReg cells (regulatory T cells) is controlled by different host factors and commensal bacteria that contribute to the development of intestinal immune homeostasis. Although it has been demonstrated that the altered Schaedler flora species, B. fragilis and disturbed Clostridia flora preferably stimulate TReg cells in the host intestine under normal conditions, stimulation of TH17/TH1 cells can occur with TReg cell deficiency. While TReg cells are induced by wild-type B. fragilis, TH17 cells are induced by polysaccharide A-mutated B. fragilis in the host intestines [80]. Various altered Schaedler flora and Clostridia species stimulate TH17/TH1 cells in the IL-10-deficient mouse model in which the functions of TReg cells are impaired [81,82]. Results indicate that while certain commensal bacteria play an immuno-suppressive role in the intestine under normal conditions, they may also have the potential to induce inflammation in other situations. The variety of commensal bacterial species that control immune homeostasis in hosts suggests that diversity in the population of gut bacteria may contribute to differences in immune responses in several conditions.