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Submitted on May 29, 2003
Accepted on September 15, 2003
1 Cedars-Sinai Medical Center-UCLA School of Medicine, Los Angeles, CA, 90048
* To whom correspondence should be addressed. E-mail: chesnokovav{at}cshs.org.
Cytokines expressed in the brain and involved in regulating the HPA axis contribute to the neuroendocrine interface. Leukemia inhibitory factor (LIF) and LIF receptors are expressed in human pituitary cells and in murine hypothalamus and pituitary. LIF potently induces pituitary POMC gene transcription and ACTH secretion and potentiates CRH induction of POMC. In vivo, LIF, along with CRH, enhances POMC expression and ACTH secretion in response to emotional and inflammatory stress. To further elucidate specific roles for both CRH and LIF in activating the inflammatory HPA response, double knockout mice (CRH/LIFKO) were generated by breeding the null mutants for each respective single gene. Inflammation produced by ip injection of LPS (1 µg/mouse) to double CRH and LIF deficient mice elicits pituitary POMC induction similar to WT, and markedly higher than in single null animals (P < 0.0.01). Double knockout mice also demonstrate robust corticosterone response to inflammation. High pituitary POMC mRNA levels may reflect abundant TNF 
, IL 1 
and IL 6 activation observed in the hypothalamus and pituitary of these animals. Our results suggest that increased central pro-inflammatory cytokine expression can compensate for the impaired HPA axis function and activates inflammatory ACTH and corticosterone responses in mice deficient in both CRH and LIF.
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