{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T06:09:20Z","timestamp":1789970960676,"version":"4.0.1"},"reference-count":35,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2013,1,1]],"date-time":"2013-01-01T00:00:00Z","timestamp":1356998400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2013,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>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-\u03b3 signaling in Campylobacter jejuni\u2013induced neutrophil accumulation and intestinal inflammation. Germ-free and specific pathogen-free Il10\u2212\/\u2212 and germ-free Il10\u2212\/\u2212;Rag2\u2212\/\u2212 mice were infected with C. jejuni (109 CFU\/mouse). PI3K-\u03b3 signaling was manipulated using either the pharmacological PI3K-\u03b3 inhibitor AS252424 (i.p. 10 mg\/kg daily) or genetically using Pi3k-\u03b3\u2212\/\u2212 mice. After up to 14 d, inflammation was assessed histologically and by measuring levels of colonic Il1\u03b2, Cxcl2, and Il17a mRNA. Neutrophils were depleted using anti-Gr1 Ab (i.p. 0.5 mg\/mouse\/every 3 d). Using germ-free Il10\u2212\/\u2212;Rag2\u2212\/\u2212 mice, we observed that innate immune cells are the main cellular compartment responsible for campylobacteriosis. Pharmacological blockade of PI3K-\u03b3 signaling diminished C. jejuni\u2013induced intestinal inflammation, neutrophil accumulation, and NF-\u03baB activity, which correlated with reduced Il1\u03b2 (77%), Cxcl2 (73%), and Il17a (72%) mRNA accumulation. Moreover, Pi3k-\u03b3\u2212\/\u2212 mice pretreated with anti\u2013IL-10R were resistant to C. jejuni\u2013induced 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\u2013induced crypt abscesses and intestinal inflammation. Our findings indicate that C. jejuni\u2013induced PI3K-\u03b3 signaling mediates neutrophil recruitment and intestinal inflammation in Il10\u2212\/\u2212 mice. Selective pharmacological inhibition of PI3K-\u03b3 may represent a novel means to alleviate severe cases of campylobacteriosis, especially in antibiotic-resistant strains.<\/jats:p>","DOI":"10.4049\/jimmunol.1201825","type":"journal-article","created":{"date-parts":[[2012,11,24]],"date-time":"2012-11-24T04:54:53Z","timestamp":1353732893000},"page":"357-365","source":"Crossref","is-referenced-by-count":42,"title":["Phosphatidylinositol 3-Kinase-\u03b3 Signaling Promotes <i>Campylobacter jejuni<\/i>\u2013Induced Colitis through Neutrophil Recruitment in Mice"],"prefix":"10.1093","volume":"190","author":[{"given":"Xiaolun","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Medicine, University of North Carolina , Chapel Hill, NC 27599"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bo","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of North Carolina , Chapel Hill, NC 27599"},{"name":"Key Laboratory of Zoonosis Research, Ministry of Education, Institute of Zoonesis, College of Animal Science and Veterinary Medicine, Jilin University , Changchun 130062,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ryan Balfour","family":"Sartor","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of North Carolina , Chapel Hill, NC 27599"},{"name":"Department of Microbiology and Immunology, University of North Carolina , Chapel Hill, NC 27599"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christian","family":"Jobin","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of North Carolina , Chapel Hill, NC 27599"},{"name":"Department of Microbiology and Immunology, University of North Carolina , Chapel Hill, NC 27599"},{"name":"Department of Pharmacology, University of North Carolina , Chapel Hill, NC 27599"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2013,1,1]]},"reference":[{"key":"2025032406220272900_r1"},{"key":"2025032406220272900_r2","doi-asserted-by":"crossref","first-page":"S103","DOI":"10.1086\/513780","article-title":"Epidemiologic and clinical features of Campylobacter jejuni infections","volume":"176","author":"Blaser","year":"1997","journal-title":"J. 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