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Grim19 attenuates DSS induced colitis in an animal model

  • Jae Kyung Kim
  • , Seung Hoon Lee
  • , Seon Young Lee
  • , Eun Kyung Kim
  • , Jeong Eun Kwon
  • , Hyeon Beom Seo
  • , Han Hee Lee
  • , Bo In Lee
  • , Sung Hwan Park
  • , Mi La Cho
  • Catholic University of Korea

Research output: Contribution to journalArticlepeer-review

19 Scopus citations

Abstract

DSS induced colitis is a chronic inflammatory disease characterized by inflammation in the gastrointestinal tract, which destabilizes the gut and induces an uncontrolled immune response. Although DSS induced colitis is generally thought to develop as a result of an abnormally active intestinal immune system, its pathogenesis remains unclear. Gene associated with retinoid interferon induced mortality (Grim) 19 is an endogenous specific inhibitor of STAT3, which regulates the expression of proinflammatory cytokines. In this study, we investigated the influence of GRIM19 in a DSS induced colitis mouse model. We hypothesized that Grim19 would ameliorate DSS induced colitis by altering STAT3 activity and intestinal inflammation. Grim19 ameliorated DSS induced colitis severity and protected intestinal tissue. The expression of STAT3 and proinflammatory cytokines such as IL-1β and TNF-α in colon and lymph nodes was decreased significantly by Grim19. Moreover, DSS induced colitis progression in a Grim19 transgenic mouse line was inhibited in association with a reduction in STAT3 and IL-17 expression. These results suggest that Grim19 attenuates DSS induced colitis by suppressing the excessive inflammatory response mediated by STAT3 activation.

Original languageEnglish
Article numbere0155853
JournalPLoS ONE
Volume11
Issue number6
DOIs
StatePublished - 1 Jun 2016

Bibliographical note

Publisher Copyright:
© 2016 Kim et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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