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Submitted on April 8, 2005
Accepted on August 15, 2005
Division of Cell Biology, Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan; Dept of Bioregulation, Institute of Development and Aging Sciences, Nippon Medical School; Third Department of Internal Medicine, Hirosaki University School of Medicine, Hirosaki 036-8562, Japan
* To whom correspondence should be addressed. E-mail: iwakura{at}ims.u-tokyo.ac.jp.
IL-1
/
and IL-6 are endogenous modulator of hypothalamo-pituitary-adrenal axis (HPAA) and are thought to play key roles in immune-neuroendocrine interactions during inflammation. Here, we show IL-1 induced a normal HPAA activation in IL-1/ KO and IL-6 KO mice at 1 h; however, at 6 h HPAA activation was reduced relative to WT mice, indicating a role for endogenous IL-1/ and IL-6 in prolonged HPAA activation. We found that the induction of proopiomelanocortin (POMC) transcript in the anterior pituitary (AP) at 6 h in response to IL-1 was reduced in IL-1/ KO and IL-6 KO mice, as well as in CRH KO mice, suggesting IL-1/, IL-6, and CRH are all required for POMC induction. The induction of CRH transcript in the paraventricular nucleus (PVN) at 6 h and plasma IL-6 levels, in response to IL-1, were reduced in IL-1/ KO mice. Since IL-1 -induced activation of STAT3 in the AP was also suppressed in IL-6 KO mice, we suggest that plasma IL-6 is first induced by IL-1, and IL-6 activates STAT3 in the AP, leading to the induction of POMC in concert with CRH. Our results suggest a role for IL-1/ in the induction of POMC in the AP through the induction of two independent pathways, CRH and IL-6.
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