20 December 2016
Campylobacter jejuni, nucleotide oligomerization domain-2, IL-10–/– infection model, IL-23/IL-22/IL-18 axis, pro-inflammatory immune responses, bacterial translocation, colonization resistance, intestinal microbiota, bifidobacteria, lactobacilli
Host immune responses are pivotal for combating enteropathogenic infections. We here assessed the impact of the innate receptor nucleotide oligomerization domain protein 2 (NOD2) in murine Campylobacter jejuni-infection. Conventionally colonized IL-10 –/– mice lacking NOD2 and IL-10 –/– controls were perorally challenged with C. jejuni strain 81-176 and displayed comparable pathogenic colonization of intestines until day 14 postinfection (p.i.). Whereas overall intestinal microbiota compositions were comparable in naive mice, NOD2 –/– IL-10 –/– mice exhibited less fecal bifidobacteria and lactobacilli than IL-10 –/– counterparts after infection. Interestingly, NOD2 –/– IL-10 –/– mice were clinically more compromised during the early phase of infection, whereas, conversely, IL-10 –/– animals exhibited more frequently bloody feces lateron. While colonic apoptotic cell and T lymphocyte numbers were comparable in either C. jejuni-infected mice, B lymphocytes were lower in the colon of infected NOD2 –/– IL-10 –/– mice versus controls. At day 14 p.i., colonic TNF and IL-23p19 mRNA levels were upregulated in NOD2 –/– IL-10 –/– mice only. Translocation rates of intestinal commensals to mesenteric lymphnodes and extra-intestinal compartments including liver and kidney were comparable, whereas viable bacteria were more frequently detected in spleens derived from IL-10 –/– as compared to NOD2 –/– IL-10 –/– mice. In conclusion, NOD2 is involved during C. jejuni infection in conventionally colonized IL-10 –/– mice in a time-dependent manner.