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Merck
  • Intestinal vitamin D receptor knockout protects from oxazolone-induced colitis.

Intestinal vitamin D receptor knockout protects from oxazolone-induced colitis.

Cell death & disease (2020-06-17)
Yongyan Shi, Ziyun Liu, Xuewei Cui, Qun Zhao, Tianjing Liu
摘要

Crohn's disease (CD) and ulcerative colitis (UC) actually had different pathological mechanisms, as the former was mainly induced by Th1 and Th17 response and the latter by Th2 response. Our previous study found that oxazolone-induced Th2-mediated colitis could not be attenuated by vitamin D supplementation. This study investigated the influence of intestinal vitamin D receptor (VDR) knockout on oxazolone-induced colitis and explored the possible immunological mechanism. Intestinal VDR knockout mice had milder oxazolone-induced colitis than wildtype controls, as demonstrated by less body weight decrease and faster recovery, more intact local structure, reduced cell apoptosis, and better preserved barrier function. Th2-mediated inflammation was significantly inhibited by VDR deficiency. Meanwhile, the percentage of invariant natural killer T (iNKT) cells did not increase as much in intestinal VDR knockout mice as in wild-type controls, nor did the iNKT cells develop normally as in the controls. Intestinal VDR knockout protected against oxazolone-induced colitis in mice by blocking Th2 cell response and reducing the function of intestinal iNKT cells. Vitamin D status had no influence on the severity of colitis. This study may explain the diverse outcomes after vitamin D supplementation in literature and add some clue to the targeted therapy of IBD.

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Sigma-Aldrich
抗 β-肌动蛋白抗体,小鼠单克隆, clone AC-15, purified from hybridoma cell culture
Sigma-Aldrich
4-乙氧基亚甲基-2-苯基-2-恶唑啉-5-酮, purified by recrystallization