ArticleGut pathogens2016
The IL-23/IL-22/IL-18 axis in murine Campylobacter jejuni infection.
Article in Gut pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 21 citations in OpenAlex.
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- 6-Formylindolo (3, 2-b) Carbazole (FICZ)-mediated protection of gut barrier is dependent on T cells in a mouse model of alcohol combined with burn injury.Biochimica et biophysica acta. Molecular basis of disease · 2020Article
- IL-23 Contributes toFrontiers in immunology · 2020Article
- Gut Microbiota and IL-17A: Physiological and Pathological Responses.Probiotics and antimicrobial proteins · 2019Review
- Impacts of Duck-Origin Parvovirus Infection on Cherry Valley Ducklings From the Perspective of Gut Microbiota.Frontiers in microbiology · 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
- Toll-Like Receptor-4 Dependent Inflammatory Responses Following Intestinal Colonization of Secondary Abiotic IL10-Deficient Mice with Multidrug-ResistantEuropean journal of microbiology & immunology · 2017Article
- Microbiota Composition and Immune Responses DuringEuropean journal of microbiology & immunology · 2017Article
- Article
- Toll-like receptor-4 differentially mediates intestinal and extra-intestinal immune responses upon multi-drug resistantGut pathogens · 2017Article
- Absence of Nucleotide-Oligomerization-Domain-2 Is Associated with Less Distinct Disease inFrontiers in cellular and infection microbiology · 2017Article
- Immune responses uponGut pathogens · 2017Article
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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
backgroundHuman Campylobacter jejuni infections are worldwide on the rise. Information about the distinct molecular mechanisms underlying campylobacteriosis, however, are scarce. In the present study we investigated whether cytokines including IL-23, IL-22 and IL-18 sharing pivotal functions in host immunity were involved in mediating immunopathological responses upon C. jejuni infection.
resultsTo address this, conventionally colonized IL-23p19(-/-), IL-22(-/-) and IL-18(-/-) mice were perorally infected with C. jejuni strain ATCC 43431. Respective gene-deficient, but not wildtype mice were susceptible to C. jejuni infection and could be readily colonized with highest pathogenic loads in the terminal ileum and colon at day 14 postinfection (p.i.). In IL-23p19(-/-), IL-22(-/-) and IL-18(-/-) mice viable C. jejuni were detected in MLNs, but did not translocate to spleen, liver, kidney and blood in the majority of cases. Susceptible IL-22(-/-), but neither IL-23p19(-/-), nor IL-18(-/-) mice harbored higher intestinal commensal E. coli loads when compared to resistant wildtype mice. Alike C. jejuni, commensal E. coli did not translocate from the intestinal to extra-intestinal tissue sites. Despite C. jejuni infection, mice lacking IL-23p19, IL-22 or IL-18 exhibited less apoptotic cells, but higher numbers of proliferating cells in their colonic epithelium as compared to wildtype mice at day 14 p.i. Less pronounced apoptosis was parallelled by lower abundance of neutrophils within the colonic mucosa and lamina propria of infected IL-23p19(-/-) and IL-22(-/-) as compared to wildtype control mice, whereas less distinct colonic TNF secretion could be measured in IL-22(-/-) and IL-18(-/-) than in wildtype mice at day 14 p.i. Notably, in infected IL-22(-/-) mice, colonic IL-23p19 mRNA levels were lower, whereas the other way round, colonic IL-22 expression rates were lower in IL-23p19(-/-) mice as compared to wildtype controls. Moreover, IL-18 mRNA was less distinctly expressed in large intestines of naive and infected IL-22(-/-) mice, but not vice versa, given that IL-22 mRNA levels did not differ between in IL-18(-/-) and wildtype mice.
conclusionCytokines belonging to the IL-23/IL-22/IL-18 axis mediate immunopathological responses upon murine C. jejuni infection in a differentially orchestrated manner. Future studies need to further unravel the underlying regulatory mechanisms orchestrating pathogenic-host interaction.
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