Adaptation of adherent-invasive E. coli to gut environment: Impact on flagellum expression and bacterial colonization ability
Gwladys Sevrin,Sébastien Massier,Benoit Chassaing,Allison Agus,Julien Delmas,Jérémy Denizot,Elisabeth Billard,Nicolas Barnich +7 more
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TLDR
Interestingly, differential flagellin regulation was observed between commensal E. coli (HS) and AIEC (LF82) strains:Flagellum expression by AIEC bacteria, in contrast to that of commensals E.E. coli, is enhanced under intestinal conditions (the presence of bile acids and mucins).Abstract:
The pathogenesis of Crohn's disease (CD) is multifactorial and involves genetic susceptibility, environmental triggers and intestinal microbiota. Adherent-invasive Escherichia coli (AIEC) are flagellated bacteria more prevalent in CD patients than in healthy subjects and promote chronic intestinal inflammation. We aim at deciphering the role of flagella and flagellin modulation by intestinal conditions. AIEC flagellum expression is required for optimal adhesion to and invasion of intestinal epithelial cells. Interestingly, differential flagellin regulation was observed between commensal E. coli (HS) and AIEC (LF82) strains: flagellum expression by AIEC bacteria, in contrast to that of commensal E. coli, is enhanced under intestinal conditions (the presence of bile acids and mucins). Flagella are involved in the ability of the AIEC LF82 strain to cross a mucus layer in vitro and in vivo, conferring a selective advantage in penetrating the mucus layer and reaching the epithelial surface. In a CEABAC10 mouse model, a non-motile mutant (LF82-ΔfliC) exhibits reduced colonization that is restored by a dextran sodium sulfate treatment that alters mucus layer integrity. Moreover, a mutant that continuously secretes flagellin (LF82-ΔflgM) triggers a stronger inflammatory response than the wild-type strain, and the mutant's ability to colonize the CEABAC10 mouse model is decreased. Overexpression of flagellin in bacteria in contact with epithelial cells can be detrimental to their virulence by inducing acute inflammation that enhances AIEC clearance. AIEC pathobionts must finely modulate flagellum expression during the infection process, taking advantage of their specific virulence gene regulation to improve their adaptability and flexibility within the gut environment.read more
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Experimental models to study intestinal microbes-mucus interactions in health and disease.
Lucie Etienne-Mesmin,Benoit Chassaing,Mickaël Desvaux,Kim De Paepe,Raphaële Gresse,Thomas Sauvaitre,Evelyne Forano,Tom Van de Wiele,Stephanie Schüller,Stephanie Schüller,Nathalie Juge,Stéphanie Blanquet-Diot +11 more
TL;DR: The structure and function of intestinal mucus and mucins, their interactions with intestinal bacteria (including commensal, probiotics and pathogenic microorganisms) and their role in modulating health and disease states are provided.
Journal ArticleDOI
Melatonin mediates mucosal immune cells, microbial metabolism, and rhythm crosstalk: A therapeutic target to reduce intestinal inflammation.
TL;DR: Unclear mechanisms and undiscovered actions of melatonin in gut‐microbiome‐immune axis are revealed and provide new insight for the outlook ofmelatonin as a potential therapeutic target in the treatment and management of intestinal diseases.
Journal ArticleDOI
Gut bacterial composition in a mouse model of Parkinson’s disease
Paula Perez-Pardo,Hemraj B. Dodiya,Philip A. Engen,Ankur Naqib,Christopher B. Forsyth,Stefan J. Green,Johan Garssen,Ali Keshavarzian,Aletta D. Kraneveld +8 more
TL;DR: Overall, intestinal bacterial dysbiosis might play an important role in both the disruption of intestinal epithelial integrity and intestinal inflammation, which could lead or contribute to the observed alpha-synuclein aggregation and PD pathology in the intestine and central nervous system in the oral rotenone mouse model of PD.
Journal ArticleDOI
Adherent-Invasive E. coli: Update on the Lifestyle of a Troublemaker in Crohn’s Disease
TL;DR: The lifestyle of AIEC bacteria within the intestine is described, from the interaction with intestinal epithelial and immune cells with an emphasis on environmental and genetic factors favoring their implantation, to their lifestyle in the intestinal lumen.
Journal ArticleDOI
Host-Specific Adaptive Diversification of Crohn's Disease-Associated Adherent-Invasive Escherichia coli.
TL;DR: The adaptive evolution of AIEC was tracked in a murine model of chronic colonization across multiple hosts and transmission events, and evolved lineages that outcompeted the ancestral strain in the host through independent mechanisms were detected.
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One-step inactivation of chromosomal genes in Escherichia coli K-12 using PCR products
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Journal ArticleDOI
Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease
Jean-Pierre Hugot,Mathias Chamaillard,Mathias Chamaillard,Habib Zouali,Suzanne Lesage,Jean-Pierre Cézard,Jacques Belaiche,Sven Almer,Curt Tysk,Colm O'Morain,Miquel A. Gassull,Vibeke Binder,Yigael Finkel,Antoine Cortot,Robert Modigliani,Pierre Laurent-Puig,C. Gower-Rousseau,J. Macry,Jean-Frederic Colombel,Mourad Sahbatou,Gilles Thomas,Gilles Thomas +21 more
TL;DR: It is suggested that the NOD2 gene product confers susceptibility to Crohn's disease by altering the recognition of these components and/or by over-activating NF-kB in monocytes, thus documenting a molecular model for the pathogenic mechanism of Crohn’s disease that can now be further investigated.
Journal ArticleDOI
A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease
Yasunori Ogura,Denise K. Bonen,Naohiro Inohara,Dan L. Nicolae,Felicia F. Chen,Richard Ramos,Heidi M. Britton,Thomas M. Moran,Reda Karaliuskas,Richard H. Duerr,Jean-Paul Achkar,Steven R. Brant,Theodore M. Bayless,Barbara S. Kirschner,Stephen B. Hanauer,Gabriel Núñez,Judy H. Cho +16 more
TL;DR: It is shown that a frameshift mutation caused by a cytosine insertion, 3020insC, which is expected to encode a truncated NOD2 protein, is associated with Crohn's disease, and a link between an innate immune response to bacterial components and development of disease is suggested.
Journal ArticleDOI
Unravelling the pathogenesis of inflammatory bowel disease
TL;DR: Recently, substantial advances in the understanding of the molecular pathogenesis of inflammatory bowel disease (IBD) have been made owing to three related lines of investigation as mentioned in this paper, which have shown the importance of epithelial barrier function, and innate and adaptive immunity in disease pathogenesis.