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      Microbiota Composition and Immune Responses During Campylobacter Jejuni Infection in Conventionally Colonized IL-10 –/– Mice Lacking Nucleotide Oligomerization Domain 2

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          Abstract

          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.

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          Most cited references 62

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          Nod2 is a general sensor of peptidoglycan through muramyl dipeptide (MDP) detection.

          Nod2 activates the NF-kappaB pathway following intracellular stimulation by bacterial products. Recently, mutations in Nod2 have been shown to be associated with Crohn's disease, suggesting a role for bacteria-host interactions in the etiology of this disorder. We show here that Nod2 is a general sensor of peptidoglycan through the recognition of muramyl dipeptide (MDP), the minimal bioactive peptidoglycan motif common to all bacteria. Moreover, the 3020insC frameshift mutation, the most frequent Nod2 variant associated with Crohn's disease patients, fully abrogates Nod2-dependent detection of peptidoglycan and MDP. Together, these results impact on the understanding of Crohn's disease development. Additionally, the characterization of Nod2 as the first pathogen-recognition molecule that detects MDP will help to unravel the well known biological activities of this immunomodulatory compound.
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            Campylobacter jejuni: molecular biology and pathogenesis.

            Campylobacter jejuni is a foodborne bacterial pathogen that is common in the developed world. However, we know less about its biology and pathogenicity than we do about other less prevalent pathogens. Interest in C. jejuni has increased in recent years as a result of the growing appreciation of its importance as a pathogen and the availability of new model systems and genetic and genomic technologies. C. jejuni establishes persistent, benign infections in chickens and is rapidly cleared by many strains of laboratory mouse, but causes significant inflammation and enteritis in humans. Comparing the different host responses to C. jejuni colonization should increase our understanding of this organism.
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              Colorectal cancer in mice genetically deficient in the mucin Muc2.

              The gastrointestinal tract is lined by a layer of mucus comprised of highly glycosylated proteins called mucins. To evaluate the importance of mucin in intestinal carcinogenesis, we constructed mice genetically deficient in Muc2, the most abundant secreted gastrointestinal mucin. Muc2-/- mice displayed aberrant intestinal crypt morphology and altered cell maturation and migration. Most notably, the mice frequently developed adenomas in the small intestine that progressed to invasive adenocarcinoma, as well as rectal tumors. Thus, Muc2 is involved in the suppression of colorectal cancer.
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                Author and article information

                Journal
                Eur J Microbiol Immunol (Bp)
                Eur J Microbiol Immunol (Bp)
                EUJMI
                European Journal of Microbiology & Immunology
                Akadémiai Kiadó (Budapest )
                2062-509X
                2062-8633
                20 December 2016
                March 2017
                : 7
                : 1
                : 1-14
                Affiliations
                Department of Microbiology and Hygiene, Charité – University Medicine Berlin , Berlin, Germany
                Author notes
                * Charité – University Medicine Berlin, CC5, Department of Microbiology and Hygiene, Campus Benjamin Franklin, FEM, Garystr. 5, D-14195 Berlin, Germany; +49-30-450524318; markus.heimesaat@ 123456charite.de

                Competing Interests

                Stefan Bereswill and Markus M. Heimesaat are Editorial Board members.

                Article
                10.1556/1886.2016.00038
                5372477
                © 2017, The Author(s)

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Page count
                Figures: 14, Tables: 0, Equations: 0, References: 56, Pages: 16
                Funding
                Founding sources: This work was supported by grants from the German Research Foundation (DFG) to A.F. and S.B. (SFB633, TP A7), M.M.H. (SFB633, TP B6), and A.E.K. and U.G. (SFB633, Immuco) and from the German Federal Ministry of Education and Research (BMBF) to S.B. (TP1.1).
                The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the article.
                Categories
                Original Article

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