Activation of the aryl hydrocarbon receptor pathway may ameliorate dextran sodium sulfate-induced colitis in mice

被引：78

作者：

Takamura, Takeyuki

Harama, Daisuke

Matsuoka, Shuji ^{[2
]}

Shimokawa, Naomi

Nakamura, Yuki

Okumura, Ko ^{[3
]}

Ogawa, Hideoki ^{[3
]}

Kitamura, Masanori ^{[4
]}

Nakao, Atsuhito ^{[1
,3
]}

机构：

[1] Univ Yamanashi, Dept Immunol, Fac Med, Chuo Ku, Yamanashi 4093898, Japan

[2] Juntendo Univ, Sch Med, Dept Pathol, Tokyo 113, Japan

[3] Juntendo Univ, Sch Med, Atopy Res Ctr, Tokyo 113, Japan

[4] Univ Yamanashi, Dept Mol Signaling, Interdisciplinary Grad Sch Med & Engn, Chuo Ku, Yamanashi 4093898, Japan

来源：

IMMUNOLOGY AND CELL BIOLOGY | 2010年 / 88卷 / 06期

关键词：

aryl hydrocarbon receptor; colitis; mouse; prostaglandin; INFLAMMATORY-BOWEL-DISEASE; PROSTAGLANDINS; EPIDEMIOLOGY; INHIBITION;

D O I：

10.1038/icb.2010.35

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The aryl hydrocarbon receptor (AhR) recognizes numerous small xenobiotic and natural molecules, such as dioxin and natural chemicals, and is involved in the metabolism of these compounds. AhR also has a regulatory role in inflammatory responses. This study investigated whether the activation of the AhR pathway affects dextran sodium sulfate (DSS)-induced colitis, an ulcerative colitis-like model, in mice. DSS-induced colitis was ameliorated by pretreatment with a potent AhR activator, 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD), in mice. In addition, the mice pretreated with TCDD showed increased prostaglandin E2 (PGE2) production in the colon, and inhibition of PGE2 production by indomethacin abrogated the inhibitory effects of TCDD on DSS-induced colitis. Collectively, the activation of the AhR pathway by TCDD may ameliorate DSS-induced colitis, at least in part, through PGE2 production. Immunology and Cell Biology (2010) 88, 685-689; doi:10.1038/icb.2010.35; published online 16 March 2010

引用

页码：685 / 689

页数：5

共 26 条

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