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Open AccessArticle

Toll-Like Receptor-4 Dependent Intestinal and Systemic Sequelae Following Peroral Campylobacter coli Infection of IL10 Deficient Mice Harboring a Human Gut Microbiota

Institute of Microbiology, Infectious Diseases and Immunology, Charité - University Medicine Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 12203 Berlin, Germany
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Author to whom correspondence should be addressed.
These authors contributed equally to this study.
Pathogens 2020, 9(5), 386; https://doi.org/10.3390/pathogens9050386
Received: 6 April 2020 / Revised: 6 May 2020 / Accepted: 14 May 2020 / Published: 18 May 2020
(This article belongs to the Special Issue Campylobacter Infections)
Zoonotic Campylobacter, including C. jejuni and C. coli, are among the most prevalent agents of food-borne enteritis worldwide. The immunopathological sequelae of campylobacteriosis are caused by Toll-like Receptor-4 (TLR4)-dependent host immune responses, induced by bacterial lipooligosaccharide (LOS). In order to investigate C. coli-host interactions, including the roles of the human gut microbiota and TLR4, upon infection, we applied a clinical acute campylobacteriosis model, and subjected secondary abiotic, TLR4-deficient IL10-/- mice and IL10-/- controls to fecal microbiota transplantation derived from human donors by gavage, before peroral C. coli challenge. Until day 21 post-infection, C. coli could stably colonize the gastrointestinal tract of human microbiota-associated (hma) mice of either genotype. TLR4-deficient IL10-/- mice, however, displayed less severe clinical signs of infection, that were accompanied by less distinct apoptotic epithelial cell and innate as well as adaptive immune cell responses in the colon, as compared to IL10-/- counterparts. Furthermore, C. coli infected IL10-/-, as opposed to TLR4-deficient IL10-/-, mice displayed increased pro-inflammatory cytokine concentrations in intestinal and, strikingly, systemic compartments. We conclude that pathogenic LOS might play an important role in inducing TLR4-dependent host immune responses upon C. coli infection, which needs to be further addressed in more detail. View Full-Text
Keywords: Toll-like Receptor-4; lipooligosaccharide; Campylobacter coli; campylobacteriosis model; host–pathogen interaction; human microbiota-associated IL-10-/- mice; pro-inflammatory immune responses; intestinal immunopathology; systemic immune responses; human gut microbiota; fecal microbiota transplantation Toll-like Receptor-4; lipooligosaccharide; Campylobacter coli; campylobacteriosis model; host–pathogen interaction; human microbiota-associated IL-10-/- mice; pro-inflammatory immune responses; intestinal immunopathology; systemic immune responses; human gut microbiota; fecal microbiota transplantation
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Kløve, S.; Genger, C.; Mousavi, S.; Weschka, D.; Bereswill, S.; Heimesaat, M.M. Toll-Like Receptor-4 Dependent Intestinal and Systemic Sequelae Following Peroral Campylobacter coli Infection of IL10 Deficient Mice Harboring a Human Gut Microbiota. Pathogens 2020, 9, 386.

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