Toll-Like Receptor-4 Is Involved in Mediating Intestinal and Extra-Intestinal Inflammation in -Infected Secondary Abiotic IL-10 Mice

Overview

Journal Microorganisms

Specialty Microbiology

Date 2020 Dec 2

PMID 33261211

Citations 7

Authors

Sigri Klove

Claudia Genger

Dennis Weschka

Soraya Mousavi

Stefan Bereswill

Markus M Heimesaat

Affiliations

Soon will be listed here.

Abstract

Human infections are emerging worldwide and constitute significant health burdens. We recently showed that the immunopathological sequelae in -infected mice were due to Toll-like receptor (TLR)-4 dependent immune responses induced by bacterial lipooligosaccharide (LOS). Information regarding the molecular mechanisms underlying -host interactions are scarce, however. Therefore, we analyzed -induced campylobacteriosis in secondary abiotic IL-10 mice with and without TLR4. Mice were infected perorally with a human isolate or with a murine commensal as apathogenic, non-invasive control. Independent from TLR4, and stably colonized the gastrointestinal tract, but only induced clinical signs of campylobacteriosis. TLR4 IL-10 mice, however, displayed less frequently fecal blood and less distinct histopathological and apoptotic sequelae in the colon versus IL-10 counterparts on day 28 following infection. Furthermore, -induced colonic immune cell responses were less pronounced in TLR4 IL-10 as compared to IL-10 mice and accompanied by lower pro-inflammatory mediator concentrations in the intestines and the liver of the former versus the latter. In conclusion, our study provides evidence that TLR4 is involved in mediating -LOS-induced immune responses in intestinal and extra-intestinal compartments during murine campylobacteriosis.

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