Morphology of segmented filamentous bacteria and their patterns of contact with the follicle-associated epithelium of the mouse terminal ileum

Caselli, Michele; Holton, John; Boldrini, Paola; Vaira, Dino; Calò, Girolamo

doi:10.4161/gmic.1.6.14390

Cited by 33 publications

(28 citation statements)

References 30 publications

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“…induce transforming growth factor ␤ (TGF-␤) production and an environment that promotes the production of colonic T regulatory cells (1), which can suppress inflammation. Conversely, uncultivable spore-forming segmented filamentous bacteria (SFB) promote the development of inflammatory Th17 cells in the small intestine and mice colonized with SFB produce higher quantities of antimicrobial defensins and are more resistant to C. rodentium infection (4,17). These studies indicate that spore-forming bacteria may be important regulators of intestinal homeostasis and that select spore-forming bacteria could prevent disease due to infection with an enteric pathogen.…”

Section: Discussionmentioning

confidence: 98%

Bacillus subtilis-Mediated Protection from Citrobacter rodentium-Associated Enteric Disease RequiresespHand Functional Flagella

Jones

Knight

2012

Infect Immun

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Commensals limit disease caused by invading pathogens; however, the mechanisms and genes utilized by beneficial microbes to inhibit pathogenesis are poorly understood. The attaching and effacing mouse pathogen Citrobacter rodentium associates intimately with the intestinal epithelium, and infections result in acute colitis. C. rodentium is used to model the human pathogens enterohemorrhagic Escherichia coli and enteropathogenic E. coli. To confirm that Bacillus subtilis, a spore-forming bacterium found in the gut of mammals, could reduce C. rodentium-associated disease, mice received wild-type B. subtilis spores and 24 h later were infected by oral gavage with pathogenic C. rodentium. Disease was assessed by determining the extent of colonic epithelial hyperplasia, goblet cell loss, diarrhea, and pathogen colonization. Mice that received wild-type B. subtilis prior to enteric infection were protected from disease even though C. rodentium colonization was not inhibited. In contrast, espH and hag mutants, defective in exopolysaccharides and flagellum production, respectively, did not protect mice from C. rodentium-associated disease. A motAB mutant also failed to protect mice from disease, suggesting that B. subtilis-mediated protection requires functional flagella. By expanding our current mechanistic knowledge of bacterial protection, we can better utilize beneficial microbes to prevent intestinal disease caused by pathogenic bacteria, ultimately reducing human disease. Our data demonstrate that wildtype B. subtilis reduced disease caused by C. rodentium infection through a mechanism that required espH and functional flagella.

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Section: Discussionmentioning

confidence: 98%

Bacillus subtilis-Mediated Protection from Citrobacter rodentium-Associated Enteric Disease RequiresespHand Functional Flagella

Jones

Knight

2012

Infect Immun

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“…The presence of these T cell subsets in the intestinal LP is profoundly influenced by specific components of the microbiota (11, 12, 22, 23), and their metabolites (22, 24) since these bacteria interact directly with intestinal epithelial cells (25) and may be sampled by underlying LP DCs and macrophages (26). The site of this steady-state CD4+ T cell differentiation has been assumed to be in the mLN based upon several key observations: 1) naïve CD4+ T cells primarily traffic through secondary lymphoid tissues and not the intestine, 2) Peyer’s patch (PP) and LP DCs migrate to the mLN where they present antigens to naïve T cells resulting in their expansion and induction of gut homing molecules (27–30), and 3) delivery of soluble antigen via the oral route induces Foxp3+ T cell differentiation in the mLN (31–33).…”

Section: Discussionmentioning

confidence: 99%

Specific Microbiota-Induced Intestinal Th17 Differentiation Requires MHC Class II but Not GALT and Mesenteric Lymph Nodes

Geem

Medina-Contreras

McBride

et al. 2014

The Journal of Immunology

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Interleukin (IL)-17 expressing CD4+ T lymphocytes (Th17 cells) naturally reside in the intestine where specific cytokines and microbiota, such as segmented filamentous bacteria (SFB), promote their differentiation. Intestinal Th17 cells are believed to initially differentiate in the GALT and/or mesenteric lymph nodes (mLN) upon antigen encounter and subsequently home to the lamina propria (LP) where they mediate effector functions. However, whether GALT and/or mLN are required for intestinal Th17 differentiation, and how microbiota containing SFB regulate antigen-specific intestinal Th17 cells remain poorly defined. Here we observed that naïve CD4+ T cells were abundant in the intestinal LP prior to weaning and that the accumulation of Th17 cells in response to microbiota containing SFB occurred in the absence of lymphotoxin (LT)-dependent lymphoid structures and the spleen. Furthermore, the differentiation of intestinal Th17 cells in the presence of microbiota containing SFB was dependent on MHC II expression by CD11c+ cells. Lastly, the differentiation of antigen-specific Th17 cells required both the presence of cognate antigen and microbiota containing SFB. These findings suggest that microbiota containing SFB create an intestinal milieu that may induce antigen-specific Th17 differentiation against food and/or bacterial antigens directly in the intestinal LP.

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“…SFB appears explosively at the time of weaning in all the animal species and colonizes the specialized epithelium and the M cells of the terminal ileum. We have previously described in detail the typical morphology of SFB and their unique pattern of contact with the terminal ileal epithelium in mice ( 5 ). Not only a clear preference of SFB for the mucosal-lymphoid specialized epithelium of the Peyer ' s patches of the terminal ileum appears evident, but also SFB directly adhere to this epithelium and penetrates within the specialized epithelial cells justifying the peculiar relationship with the immune system.…”

Section: Segmented Filamentous Bacteria-like Organisms In Histologicamentioning

confidence: 95%

Segmented Filamentous Bacteria-Like Organisms in Histological Slides of Ileo-Cecal Valves in Patients with Ulcerative Colitis

Caselli

Tosini

Gafà

et al. 2013

American Journal of Gastroenterology

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Morphology of segmented filamentous bacteria and their patterns of contact with the follicle-associated epithelium of the mouse terminal ileum

Cited by 33 publications

References 30 publications

Bacillus subtilis-Mediated Protection from Citrobacter rodentium-Associated Enteric Disease RequiresespHand Functional Flagella

Bacillus subtilis-Mediated Protection from Citrobacter rodentium-Associated Enteric Disease RequiresespHand Functional Flagella

Specific Microbiota-Induced Intestinal Th17 Differentiation Requires MHC Class II but Not GALT and Mesenteric Lymph Nodes

Segmented Filamentous Bacteria-Like Organisms in Histological Slides of Ileo-Cecal Valves in Patients with Ulcerative Colitis

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