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This version published online on September 23, 2004
Endocrinology, doi:10.1210/en.2004-0946
A more recent version of this article appeared on January 1, 2005
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Submitted on July 22, 2004
Accepted on September 13, 2004

MACROPHAGE MIGRATION INHIBITORY FACTOR IS RELEASED FROM PITUITARY FOLLICULO-STELLATE-LIKE CELLS BY ENDOTOXIN AND DEXAMETHASONE AND ATTENUATES THE STEROID-INDUCED INHIBITION OF INTERLEUKIN 6 RELEASE

Tanya Tierney, Reshma Patel, Caroline A S Stead, Lin Leng, Richard Bucala, and Julia C Buckingham*

Department of Cellular and Molecular Neuroscience, Division of Neuroscience and Psychological Medicine, Faculty of Medicine, Imperial College London, Commonwealth Building, Hammersmith Campus, Du Cane Road, London W12 0NN, UK.; Department of Internal Medicine and Pathology, Yale University School of Medicine, New Haven, CT 06520, USA

* To whom correspondence should be addressed. E-mail: j.buckingham{at}imperial.ac.uk.

Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine produced by peripheral immune cells and also by endocrine cells in the anterior pituitary gland. MIF exerts its pro-inflammatory actions in the host defense system by blocking the inhibitory effects of glucocorticoids on the release of other pro-inflammatory cytokines (e.g. IL-1, IL-6, TNF{alpha}). Reports that pituitary folliculo-stellate (FS) cells share many characteristics with immune cells, led us to propose that these cells may serve as an additional source of MIF in the pituitary and that pituitary-derived MIF may act in an autocrine or paracrine manner to modulate endotoxin-induced cytokine release from FS cells. In the present study we addressed this hypothesis by using (a) immunohistochemistry to localize MIF in primary pituitary tissue and (b) well characterized FS (TtT/GF), corticotroph (AtT20) and macrophage/monocyte (RAW 264.7) cell lines to explore the effects of CRH, endotoxin and dexamethasone on MIF release and to examine the effects of MIF on IL-6 release. Our immunohistochemical study showed that MIF is expressed in abundance in S100-positive FS cells and also in other pituitary cell types. All three cell lines expressed MIF protein and responded to endotoxin (10 - 1000ng/ml, 24 h) and dexamethasone (100 pM - 10 nM, 24 h) with concentration-dependent increases in MIF release. CRH (10 - 100 nM) also stimulated MIF release from AtT20 cells but, unlike endotoxin and dexamethasone, it had no effect on MIF release from TtT/GF or RAW cells. Recombinant MIF did not affect the basal release of interleukin 6 (IL-6) from TtT/GF cells; however, it effectively reversed the inhibitory effects of dexamethasone (1 nM) on the endotoxin-induced release of IL-6 from these cells. The results suggest that the FS cells are both a source of and a target for MIF and raise the possibility that MIF serves as a paracrine/autocrine factor in the pituitary gland that contributes to the protective neuroendocrine response to endotoxin.
Key words: Macrophage migration inhibitory factor (MIF) • Immune-neuroendocrine interactions • Anterior pituitary • Folliculo-stellate cells • Interleukin-6 • Glucocorticoids • Endotoxin • Corticotrophin (ACTH) • Hypothalamo-pituitary-adrenocortical (HPA) axis




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