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Toll-Like Receptor-4 Is Involved in Mediating Intestinal and Extra-Intestinal Inflammation in Campylobacter coli -Infected Secondary Abiotic IL-10 -/- Mice.
- Source :
-
Microorganisms [Microorganisms] 2020 Nov 27; Vol. 8 (12). Date of Electronic Publication: 2020 Nov 27. - Publication Year :
- 2020
-
Abstract
- Human Campylobacter infections are emerging worldwide and constitute significant health burdens. We recently showed that the immunopathological sequelae in Campylobacter jejuni -infected mice were due to Toll-like receptor (TLR)-4 dependent immune responses induced by bacterial lipooligosaccharide (LOS). Information regarding the molecular mechanisms underlying Campylobacter coli -host interactions are scarce, however. Therefore, we analyzed C. coli -induced campylobacteriosis in secondary abiotic IL-10 <superscript>-/-</superscript> mice with and without TLR4. Mice were infected perorally with a human C. coli isolate or with a murine commensal Escherichia coli as apathogenic, non-invasive control. Independent from TLR4, C. coli and E. coli stably colonized the gastrointestinal tract, but only C. coli induced clinical signs of campylobacteriosis. TLR4 <superscript>-/-</superscript> IL-10 <superscript>-/-</superscript> mice, however, displayed less frequently fecal blood and less distinct histopathological and apoptotic sequelae in the colon versus IL-10 <superscript>-/-</superscript> counterparts on day 28 following C. coli infection. Furthermore, C. coli -induced colonic immune cell responses were less pronounced in TLR4 <superscript>-/-</superscript> IL-10 <superscript>-/-</superscript> as compared to IL-10 <superscript>-/-</superscript> 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 C. coli -LOS-induced immune responses in intestinal and extra-intestinal compartments during murine campylobacteriosis.
Details
- Language :
- English
- ISSN :
- 2076-2607
- Volume :
- 8
- Issue :
- 12
- Database :
- MEDLINE
- Journal :
- Microorganisms
- Publication Type :
- Academic Journal
- Accession number :
- 33261211
- Full Text :
- https://doi.org/10.3390/microorganisms8121882