title: Interleukin 19 reduces inflammation in chemically induced experimental colitis.
abstract: Inflammatory bowel disease results from chronic dysregulation of the mucosal immune system and aberrant activation of both the innate and adaptive immune responses. Interleukin (IL)-19, a member of the IL-10 family, functions as an anti-inflammatory cytokine. Here, we investigated the contribution of IL-19 to intestinal inflammation in a model of T cell-mediated colitis in mice. Inflammatory responses in IL-19-deficient mice were assessed using the 2,4,6-trinitrobenzene sulfonic acid (TNBS) model of acute colitis. IL-19 deficiency aggravated TNBS-induced colitis and compromised intestinal recovery in mice. Additionally, the exacerbation of TNBS-induced colonic inflammation following genetic ablation of IL-19 was accompanied by increased production of interferon-gamma, IL-12 (p40), IL-17, IL-22, and IL-33, and decreased production of IL-4. Moreover, the exacerbation of colitis following IL-19 knockout was also accompanied by increased production of CXCL1, G-CSF and CCL5. Using this model of induced colitis, our results revealed the immunopathological relevance of IL-19 as an anti-inflammatory cytokine in intestinal inflammation in mice.
authors.affiliation: Laboratory of Veterinary Pharmacology, Division of Veterinary Science, Osaka Prefecture University Graduate School of Life and Environmental Science, Izumisano, Osaka 598-8531, Japan.
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Matsuo
authors.affiliation: Laboratory of Veterinary Pharmacology, Division of Veterinary Science, Osaka Prefecture University Graduate School of Life and Environmental Science, Izumisano, Osaka 598-8531, Japan. Electronic address: azuma@vet.osakafu-u.ac.jp.
authors.forename: Yasu-Taka
authors.initials: YT
authors.lastname: Azuma
authors.affiliation: Laboratory of Veterinary Pathology, Division of Veterinary Science, Osaka Prefecture University Graduate School of Life and Environmental Science, Izumisano, Osaka 598-8531, Japan.
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Kuwamura
authors.affiliation: Laboratory of Toxicology, Setsunan University Faculty of Pharmaceutical Sciences, Hirakata, Osaka 573-0101, Japan.
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Kuramoto
authors.affiliation: Laboratory of Veterinary Pharmacology, Division of Veterinary Science, Osaka Prefecture University Graduate School of Life and Environmental Science, Izumisano, Osaka 598-8531, Japan.
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Nishiyama
authors.affiliation: Laboratory of Veterinary Pharmacology, Division of Veterinary Science, Osaka Prefecture University Graduate School of Life and Environmental Science, Izumisano, Osaka 598-8531, Japan.
authors.forename: Natsuho
authors.initials: N
authors.lastname: Yoshida
authors.affiliation: Laboratory of Veterinary Pharmacology, Division of Veterinary Science, Osaka Prefecture University Graduate School of Life and Environmental Science, Izumisano, Osaka 598-8531, Japan.
authors.forename: Yoshihito
authors.initials: Y
authors.lastname: Ikeda
authors.affiliation: Laboratory of Veterinary Pharmacology, Division of Veterinary Science, Osaka Prefecture University Graduate School of Life and Environmental Science, Izumisano, Osaka 598-8531, Japan.
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Fujimoto
authors.affiliation: Laboratory of Veterinary Pharmacology, Division of Veterinary Science, Osaka Prefecture University Graduate School of Life and Environmental Science, Izumisano, Osaka 598-8531, Japan.
authors.forename: Hidemitsu
authors.initials: H
authors.lastname: Nakajima
authors.affiliation: Laboratory of Veterinary Pharmacology, Division of Veterinary Science, Osaka Prefecture University Graduate School of Life and Environmental Science, Izumisano, Osaka 598-8531, Japan.
authors.forename: Tadayoshi
authors.initials: T
authors.lastname: Takeuchi
mesh_terms: D000818:Animals; D003092:Colitis / Q000139:chemically induced* / Q000235:genetics* / Q000473:pathology; D003424:Crohn Disease / Q000139:chemically induced / Q000473:pathology; D016207:Cytokines / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D007249:Inflammation / Q000139:chemically induced* / Q000235:genetics*; D016753:Interleukin-10 / Q000235:genetics*; D007378:Interleukins; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D020127:Recovery of Function; D013601:T-Lymphocytes / Q000276:immunology; D014302:Trinitrobenzenesulfonic Acid
chemical_list: D016207:Cytokines; C498891:Il19 protein, mouse; D007378:Interleukins; D016753:Interleukin-10; D014302:Trinitrobenzenesulfonic Acid
keywords: Anti-inflammatory cytokine; Colitis; IL-19; Inflammatory bowel disease