ArticleEuropean journal of microbiology & immunology2016
The Role of IL-23, IL-22, and IL-18 in Campylobacter Jejuni Infection of Conventional Infant Mice.
Article in European journal of microbiology & immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Effects of Sublethally Injured Campylobacter jejuni in Mice.Microbiology spectrum · 2022Article
- IL-23 Contributes toFrontiers in immunology · 2020Article
- Neutrophil extracellular traps (NETs) exacerbate severity of infant sepsis.Critical care (London, England) · 2019Article
- Multidrug-ResistantFrontiers in immunology · 2019Article
- Comprehensive Kinetic Survey of Intestinal, Extra-Intestinal and Systemic Sequelae of Murine Ileitis Following Peroral Low-DoseFrontiers in cellular and infection microbiology · 2019Article
- Microbiota Composition and Immune Responses DuringEuropean journal of microbiology & immunology · 2017Article
- Toll-like receptor-4 differentially mediates intestinal and extra-intestinal immune responses upon multi-drug resistantGut pathogens · 2017Article
- Article
- Colonic Expression of Genes Encoding Inflammatory Mediators and Gelatinases During Campylobacter Jejuni Infection of Conventional Infant Mice.European journal of microbiology & immunology · 2016Article
- Interleukin-18 Mediates Immune Responses to Campylobacter jejuni Infection in Gnotobiotic Mice.PloS one · 2016Article
- The IL-23/IL-22/IL-18 axis in murine Campylobacter jejuni infection.Gut pathogens · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have recently shown that, within 1 week following peroral Campylobacter jejuni infection, conventional infant mice develop self-limiting enteritis. We here investigated the role of IL-23, IL-22, and IL-18 during C. jejuni strain 81-176 infection of infant mice. The pathogen efficiently colonized the intestines of IL-18(-/-) mice only, but did not translocate to extra-intestinal compartments. At day 13 postinfection (p.i.), IL-22(-/-) mice displayed lower colonic epithelial apoptotic cell numbers as compared to wildtype mice, whereas, conversely, colonic proliferating cells increased in infected IL-22(-/-) and IL-18(-/-) mice. At day 6 p.i., increases in neutrophils, T and B lymphocytes were less pronounced in gene-deficient mice, whereas regulatory T cell numbers were lower in IL-23p19(-/-) and IL-22(-/-) as compared to wildtype mice, which was accompanied by increased colonic IL-10 levels in the latter. Until then, colonic pro-inflammatory cytokines including TNF, IFN-γ, IL-6, and MCP-1 increased in IL-23p19(-/-) mice, whereas IL-18(-/-) mice exhibited decreased cytokine levels and lower colonic numbers of T and B cell as well as of neutrophils, macrophages, and monocytes as compared to wildtype controls. In conclusion, IL-23, IL-22, and IL-18 are differentially involved in mediating C. jejuni-induced immunopathology of conventional infant mice.
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