Modulation of type IIL-1 receptor and IL-1β mRNA expression followed by endotoxin treatment in the corticotropin-releasing hormone-deficient mouse

被引:13
|
作者
Nazarloo, HP [1 ]
Takao, T [1 ]
Taguchi, T [1 ]
Ito, H [1 ]
Hashimoto, K [1 ]
机构
[1] Kochi Med Sch, Dept Internal Med 2, Nankoku, Kochi 7838505, Japan
关键词
IL-1; CRH KO; LPS;
D O I
10.1016/S0165-5728(03)00176-0
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
In an attempt to define the possible role of corticotropin-releasing hormone (CRH) on lipopolysaccharide (LPS)-induced type 1 interleukin-1 receptor (IL-1R1), IL-1alpha, and IL-1beta mRNAs in the pituitary, adrenal gland and spleen, we used CRH-deficient (knockout, KO) mouse in this study. LPS administration resulted in a robust increase in IL-1R1 mRNA levels in the pituitary, adrenal gland and spleen of wild-type (WT) and CRH KO mice, but this elevation was attenuated in the pituitary and adrenal gland of CRH KO mice. CRH deficiency did not affect LPS administration induced increase of IL-1alpha mRNA as well as IL-1beta mRNA in the pituitary and adrenal gland. Lack of CRH attenuated LPS administration induced increase of IL-1beta mRNA expression in the spleen. These data demonstrate the pivotal and organspecific modulation of CRH for IL-1 and IL-1R1 mRNAs following endotoxin treatment. (C) 2003 Elsevier B.V. All rights reserved.
引用
收藏
页码:102 / 108
页数:7
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