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Submitted on October 24, 2003
Accepted on December 12, 2003
1 Department of Endocrine- and Behavioral Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest H-1083 Hungary; Department of Physiology and Biochemistry, Faculty of Veterinary Science, Szent István University, H-1400 Budapest, Hungary.; Thyroid Section, Division of Endocrinology, Diabetes and Hypertension Brigham and Women's Hospital and Harvard Medical School, Boston, MA USA; Tupper Research Institute and Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, Tufts-New England Medical Center, Boston, MA 02111; Department of Community Health, Tufts University School of Medicine, Boston, MA 02111; Division of Endocrinology, University of Massachusetts Medical School, Worcester, MA 01655; Department of Neuroscience, Tufts University School of Medicine, Boston, MA 02111
* To whom correspondence should be addressed. E-mail: rlechan{at}tufts-nemc.org.
To determine whether the type 2 iodothyronine deiodinase (D2), the principal CNS enzyme converting T4 to biologically active T3, is regulated in tanycytes by immune activation, D2 activity was measured in the mediobasal hypothalamus (MBH) 4, 12, and 24 h following administration of bacterial lipopolysaccharide (LPS) and compared with D2 levels in the cortex and anterior pituitary of rats. In contrast to D2 activity in the cortex and anterior pituitary that showed a steady linear increase over 24 h, coincident with a decline in thyroid hormone and TSH levels, D2 activity peaked in the MBH 12 h following LPS administration. By in situ hybridization, the increased D2 mRNA synthesis induced by LPS was specifically localized to tanycytes lining the third ventricle. In vitro assays in HC11 and HEK-293 cells demonstrated that the p65 subunit of NF-
B markedly increased both rat and human D2 genes (dio2) as analyzed by promoter assays. No activation of human dio2 was observed when an 83 bp minimal promoter was used. We propose that LPS or LPS-induced cytokines directly induce D2 mRNA in tanycytes. The ensuing MBH-specific D2-mediated local thyrotoxicosis may suppress the HPT axis by local feedback inhibition of hypophysiotropic TRH and/or TSH and contribute to the mechanism of central hypothyroidism associated with infection.
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