Interleukin 19 reduces inflammation in chemically induced experimental colitis

Yukiko Matsuo, Yasu Taka Azuma, Mitsuru Kuwamura, Nobuyuki Kuramoto, Kazuhiro Nishiyama, Natsuho Yoshida, Yoshihito Ikeda, Yasuyuki Fujimoto, Hidemitsu Nakajima, Tadayoshi Takeuchi

Research output: Contribution to journalArticlepeer-review

24 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)468-475
Number of pages8
JournalInternational Immunopharmacology
Issue number2
Publication statusPublished - Dec 1 2015
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Pharmacology


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