Enhanced pro-inflammatory cytokine production in Gαi2-deficient mice on colitis prone and colitis resistant 129Sv genetic backgrounds

被引：13

作者：

Bjursten, M ^{[1
]}

Hultgren, OH ^{[1
]}

Hörnquist, EH ^{[1
]}

机构：

[1] Gothenburg Univ, Dept Clin Immunol, S-41346 Gothenburg, Sweden

来源：

CELLULAR IMMUNOLOGY | 2004年 / 228卷 / 02期

关键词：

IBD; colitis; G alpha i2; staphylococcus; superantigen;

D O I：

10.1016/j.cellimm.2004.05.001

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Mice deficient in G-protein subunit alphai2 develop colitis closely resembling human ulcerative colitis when raised on 129SvEv background. When backcrossing the Galphai2-deficiency into a 129SvJBom genetic background, surprisingly, mice did not develop colitis. In vitro stimulation of splenocytes with formalin-killed Staphylococcus aureus resulted in significantly increased production of interleukin-1beta, tumor necrosis factor, and interleukin-12p40 in Galphai2(-/-) as compared to control mice. The enhanced production of proinflammatory cytokines was seen in colitis prone as well as in colitis resistant genetic background. A similar outcome was seen upon stimulation with toxic shock syndrome toxin-1, a T cell superantigen, except that Galphai2(-/-) colitis resistant 129SvJBom splenocytes did not show increased production of IL-12p40 as compared to their controls. (C) 2004 Elsevier Inc. All rights reserved.

引用

页码：77 / 80

页数：4

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