ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Phosphatidylinositol 3-kinase-γ signaling promotes Campylobacter jejuni-induced colitis through neutrophil recruitment in mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 45 citations in OpenAlex.
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- Tofacitinib ameliorates Campylobacter-induced intestinal pathology by suppressing IFNγ producing ILCs and T cells.Mucosal immunology · 2025Article
- The Mechanistic Target of Rapamycin MediatesMicroorganisms · 2025Article
- The Role of PI3k-Gamma Modulation in Bacterial Infection: A Review of the Literature and Selected Experimental Observations.Antibiotics (Basel, Switzerland) · 2025Review
- Oral treatment of human gut microbiota associated IL-10Frontiers in microbiology · 2024Article
- Oral application of carvacrol, butyrate, ellagic acid, and 2'-fucosyl-lactose to mice suffering from acute campylobacteriosis - Results from a preclinical placebo-controlled intervention study.European journal of microbiology & immunology · 2023Article
- A secreted sirtuin fromScience advances · 2023Article
- Vaccines UsingMicroorganisms · 2022Article
- Article
- The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colitis through modulation of P2X4 receptor-dependent metabolism in myeloid cells.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Host Cellular Immune Response to Infection by Campylobacter Spp. and Its Role in Disease.Infection and immunity · 2021Review
- Campylobacter infection promotes IFNγ-dependent intestinal pathology via ILC3 to ILC1 conversion.Mucosal immunology · 2021Article
- Murine Models for the Investigation of Colonization Resistance and Innate Immune Responses in Campylobacter Jejuni Infections.Current topics in microbiology and immunology · 2021Article
- Microbiota attenuates chicken transmission-exacerbated campylobacteriosis in Il10Scientific reports · 2020Article
- Induction of neutrophil extracellular traps by Campylobacter jejuni.Cellular microbiology · 2020Article
- LINC01116 promotes tumor proliferation and neutrophil recruitment via DDX5-mediated regulation of IL-1β in glioma cell.Cell death & disease · 2020Article
- Novel ClinicalMicroorganisms · 2020Review
- Gut Fecal Microbiota Transplant in a Mouse Model of Orthotopic Rectal Cancer.Frontiers in oncology · 2020Article
- IL-23 Contributes toFrontiers in immunology · 2020Article
- Characterization of ecotin homologs from Campylobacter rectus and Campylobacter showae.PloS one · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Crypt abscesses caused by excessive neutrophil accumulation are prominent features of human campylobacteriosis and its associated pathology. The molecular and cellular events responsible for this pathological situation are currently unknown. We investigated the contribution of PI3K-γ signaling in Campylobacter jejuni-induced neutrophil accumulation and intestinal inflammation. Germ-free and specific pathogen-free Il10(-/-) and germ-free Il10(-/-);Rag2(-/-) mice were infected with C. jejuni (10(9) CFU/mouse). PI3K-γ signaling was manipulated using either the pharmacological PI3K-γ inhibitor AS252424 (i.p. 10 mg/kg daily) or genetically using Pi3k-γ(-/-) mice. After up to 14 d, inflammation was assessed histologically and by measuring levels of colonic Il1β, Cxcl2, and Il17a mRNA. Neutrophils were depleted using anti-Gr1 Ab (i.p. 0.5 mg/mouse/every 3 d). Using germ-free Il10(-/-);Rag2(-/-) mice, we observed that innate immune cells are the main cellular compartment responsible for campylobacteriosis. Pharmacological blockade of PI3K-γ signaling diminished C. jejuni-induced intestinal inflammation, neutrophil accumulation, and NF-κB activity, which correlated with reduced Il1β (77%), Cxcl2 (73%), and Il17a (72%) mRNA accumulation. Moreover, Pi3k-γ(-/-) mice pretreated with anti-IL-10R were resistant to C. jejuni-induced intestinal inflammation compared with Wt mice. This improvement was accompanied by a reduction of C. jejuni translocation into the colon and extraintestinal tissues and by attenuation of neutrophil migratory capacity. Furthermore, neutrophil depletion attenuated C. jejuni-induced crypt abscesses and intestinal inflammation. Our findings indicate that C. jejuni-induced PI3K-γ signaling mediates neutrophil recruitment and intestinal inflammation in Il10(-/-) mice. Selective pharmacological inhibition of PI3K-γ may represent a novel means to alleviate severe cases of campylobacteriosis, especially in antibiotic-resistant strains.
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