Abstract
In an attempt to define the possible role of corticotropin-releasing hormone (CRH) on lipopolysaccharide (LPS)-induced type I interleukin-1 receptor (IL-1R1), IL-1α, and IL-1β 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-1α mRNA as well as IL-1β mRNA in the pituitary and adrenal gland. Lack of CRH attenuated LPS administration induced increase of IL-1β mRNA expression in the spleen. These data demonstrate the pivotal and organ-specific modulation of CRH for IL-1 and IL-1R1 mRNAs following endotoxin treatment.
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