Home Contact 사이트맵
 
 
HOME > 커뮤니티 > 우수논문소식
서동혁 Xiumei Che(내과학교실) Sci Rep
등록일 : 2017-04-18 오후 5:59:00       조회 : 467
첨   부 :
공동제1저자 서동혁(내과학교실, BK21), Xiumei Che(내과학교실, BK21 졸업), 곽민섭(경희대)
공동교신저자 김승원 천재희(내과학교실)

Sci Rep. 2017 Apr 12ɕ(1):851. doi: 10.1038/s41598-017-00840-2.
Interleukin-33 regulates intestinal inflammation by modulating macrophages in inflammatory bowel disease.

Seo DH1,2,3, Che X1,2,3, Kwak MS4,5, Kim S1,3, Kim JH1,2, Ma HW1,2, Kim DH1,3, Kim TI1, Kim WH1, Kim SW6,7,8, Cheon JH9,10,11.
Author information
1Department of Internal Medicine and Institute of Gastroenterology, Yonsei University College of Medicine, Seoul, Korea.
2Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.
3Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea.
4Department of Internal Medicine, Graduate School, Yonsei University College of Medicine, Seoul, Korea.
5Department of Internal Medicine, Kyung Hee University Hospital at Gang Dong, Kyung Hee University School of Medicine, Seoul, Korea.
6Department of Internal Medicine and Institute of Gastroenterology, Yonsei University College of Medicine, Seoul, Korea. swk21c@hanmail.net.
7Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea. swk21c@hanmail.net.
8Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea. swk21c@hanmail.net.
9
Department of Internal Medicine and Institute of Gastroenterology, Yonsei University College of Medicine, Seoul, Korea. GENIUSHEE@yuhs.ac.
10
Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea. GENIUSHEE@yuhs.ac.
11
Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea. GENIUSHEE@yuhs.ac.
Abstract
Interleukin 33 (IL-33) that signals through the ST2 receptor has emerged as a critical modulator in several inflammatory disorders, including inflammatory bowel disease (IBD). However, the precise mechanisms by which IL-33 modulates IBD are controversial. The aim of this study was thus to clarify the role of IL-33 in IBD. The plasma levels of IL-33 were significantly decreased, but soluble ST2 levels were increased in patients with IBD compared to healthy individuals. Moreover, IL-33 restored goblet cell numbers and induced macrophage switching from the M1 to the M2 phenotype. These effects were sufficient to ameliorate colitis in dextran sodium sulfate, trinitrobenzene sulfonic acid, and peritoneal cavity cell transfer models. IL-33 facilitated goblet cell restoration via modulating macrophages toward the M2 phenotype. In addition, wound healing was significantly faster in IL-33-treated human monocyte-derived macrophages than in control cells, which could be attributed to increased polarisation into M2 macrophages. We found that patients with IBD show decreased serum levels of IL-33 compared with healthy individuals and that IL-33 can attenuate colitis and aid tissue repair in mice. The mechanism by which IL-33 exerts these effects appears to involve the stimulation of differentiation of goblet cells and M2 macrophages.
이유라(의생명과학부) Oncotarget 2017-05-12
양정민 유제욱(미생물학교실) Front Immunol 2017-04-15