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Neuroendocrine Research Laboratory, Departments of Psychiatry and Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania 19104
Address all correspondence and requests for reprints to: Eva Redei, Department of Psychiatry, Northwestern University Medical School, 303 East Chicago Avenue, 9–176, Chicago, Illinois 60611-3008. E-mail: e-redei{at}nwu.edu
Administration of streptococcal cell wall (SCW) preparation induces an
inflammatory response in susceptible animals that is a model frequently
used for rheumatoid arthritis. The degree of inflammation produced by
SCW is greatly enhanced by low endogenous levels of glucocorticoids due
to diminished hypothalamic-pituitary-adrenal activity. Because
decreased glucocorticoid production is known to occur in the
hypothyroid state, we tested whether hypothyroidism would increase, and
conversely, whether hyperthyroidism would decrease, the inflammatory
responses to SCW. Adult female Sprague Dawley rats were fed a regular
diet (control), L-T4 (T4; hyperthyroid), or
6-propyl-thiouracil (hypothyroid) in drinking water for 7 weeks.
Hypothyroidism resulted in elevated plasma levels of TSH and
hypothalamic preproTRH messenger RNA (mRNA) while reducing anterior
pituitary POMC mRNA and plasma ACTH and corticosterone levels. In
contrast, hyperthyroid rats produced opposite results: decreased
measures of central thyroid function but increased pituitary-adrenal
function. Three days after administration of SCW, macrophage
inflammatory protein-1
and interleukin-1ß mRNA expression
increased dramatically in controls and even further in hypothyroid
animals, as measured by Northern blot analysis. In contrast,
T4-treated rats showed significant inhibition of these
inflammatory markers. Thus, the hyperthyroid state combined with
increased endogenous glucocorticoid levels is protective against
inflammatory challenges. The inverse relationship between preproTRH
expression and pituitary-adrenal function suggests the possibility of a
direct inhibitory link connecting the hypothalamic-pituitary-adrenal
and thyroid axes, and suggests alternative sites of therapeutic
intervention for rheumatoid arthritis and other inflammatory associated
disorders.
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