ArticleMicrobial pathogenesis2008
Genetic background of IL-10(-/-) mice alters host-pathogen interactions with Campylobacter jejuni and influences disease phenotype.
Article in Microbial pathogenesis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
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- Th1/Th17-mediated Immunity and Protection from Peripheral Neuropathy in Wildtype and IL10Comparative medicine · 2022Article
- Murine Models for the Investigation of Colonization Resistance and Innate Immune Responses in Campylobacter Jejuni Infections.Current topics in microbiology and immunology · 2021Article
- Innate Lymphoid Cells in Response to Intracellular Pathogens: ProtectionFrontiers in cellular and infection microbiology · 2021Review
- Microbiota attenuates chicken transmission-exacerbated campylobacteriosis in Il10Scientific reports · 2020Article
- Influence of Genetic Background and Sex on Gene Expression in the Mouse (Comparative medicine · 2020Article
- Metagenomic Analysis of the Gut Microbiota of Wild Mice, a Newly Identified Reservoir ofFrontiers in cellular and infection microbiology · 2020Article
- IL-23 Contributes toFrontiers in immunology · 2020Article
- Transplanted human fecal microbiota enhanced Guillain Barré syndrome autoantibody responses after Campylobacter jejuni infection in C57BL/6 mice.Microbiome · 2017Article
- Article
- Contrasting immune responses mediate Campylobacter jejuni-induced colitis and autoimmunity.Mucosal immunology · 2014Article
- Phosphatidylinositol 3-kinase-γ signaling promotes Campylobacter jejuni-induced colitis through neutrophil recruitment in mice.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Article
- Outcome of infection of C57BL/6 IL-10(-/-) mice with Campylobacter jejuni strains is correlated with genome content of open reading frames up- and down-regulated in vivo.Microbial pathogenesis · 2013Article
- Passage of Campylobacter jejuni through the chicken reservoir or mice promotes phase variation in contingency genes Cj0045 and Cj0170 that strongly associates with colonization and disease in a mouse model.Microbiology (Reading, England) · 2012Article
- Campylobacter jejuni induces acute enterocolitis in gnotobiotic IL-10-/- mice via Toll-like-receptor-2 and -4 signaling.PloS one · 2012Article
- What you eat is what you get: Novel Campylobacter models in the quadrangle relationship between nutrition, obesity, microbiota and susceptibility to infection.European journal of microbiology & immunology · 2011Article
- Article
- Gnotobiotic IL-10; NF-kappaB mice develop rapid and severe colitis following Campylobacter jejuni infection.PloS one · 2009Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
We hypothesized that particular genetic backgrounds enhance rates of colonization, increase severity of enteritis, and allow for extraintestinal spread when inbred IL-10(-/-) mice are infected with pathogenic C. jejuni. Campylobacter jejuni stably colonized C57BL/6 and NOD mice, while congenic strains lacking IL-10 developed typhlocolitis following colonization that mimicked human campylobacteriosis. However, IL-10 deficiency alone was not necessary for the presence of C. jejuni in extraintestinal sites. C3H/HeJ tlr4(-/-) mice that specifically express the Cdcs1 allele showed colonization and limited extraintestinal spread without enteritis implicating this interval in the clinical presentation of C. jejuni infection. Furthermore, when the IL-10 gene is inactivated as in C3Bir tlr4(-/-) IL-10(-/-) mice, enteritis and intensive extraintestinal spread were observed, suggesting that clinical presentations of C. jejuni infection are controlled by a complex interplay of factors. These data demonstrate that lack of IL-10 had a greater effect on C. jejuni induced colitis than other immune elements such as TLR4 (C3H/HeJ, C3Bir IL-10(-/-)), MHC H-2g7, diabetogenic genes, and CTLA-4 (NOD) and that host genetic background is in part responsible for disease phenotype. C3Bir IL-10(-/-) mice where Cdcs1 impairs gut barrier function provide a new murine model of C. jejuni and can serve as surrogates for immunocompromised patients with extraintestinal spread.
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