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−/− 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−/− 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 C. coli infection. Furthermore, C. coli-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 C. coli-LOS-induced immune responses in intestinal and extra-intestinal compartments during murine campylobacteriosis.
Highlights
Campylobacter infections are among the most prevalent causes of bacterial infectious gastroenteritis worldwide [1,2]
Data collected in the framework of a population-based sentinel surveillance scheme for Campylobacter infections in the United Kingdom revealed, for instance, that C. coli was the causative agent in 25,000 gastroenteritis cases with 11 lethal outcomes [12]
Comparable E. coli numbers could be cultivated from luminal samples taken from stomach, duodenum, ileum, and colon of TLR4−/− IL-10−/− as compared to IL-10−/− mice (not significant (n.s.); Figure 2A), which held true for C. coli, except for gastric luminal C. coli loads that were approximately two orders of magnitude higher in the former as compared to the latter at day 28 post-challenge (p < 0.001; Figure 2B)
Summary
Campylobacter infections are among the most prevalent causes of bacterial infectious gastroenteritis worldwide [1,2]. C. jejuni and, less frequently, C. coli induce the diarrheal disease complex campylobacteriosis in infected human patients. Raw or undercooked meat from livestock, such as poultry, cattle, pigs, and sheep, are common sources of C. jejuni and C. coli transmission to humans [8,9]. In contaminated sheep and pig meat, for instance, most Campylobacter isolates have been identified as C. coli [8,10]. Data collected in the framework of a population-based sentinel surveillance scheme for Campylobacter infections in the United Kingdom revealed, for instance, that C. coli was the causative agent in 25,000 gastroenteritis cases with 11 lethal outcomes [12]
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