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Abstract
A subgroup of individuals with major depressive disorder have an impaired thyrotropin
(TSH) response to thyrotropin-releasing hormone (TRH). The molecular relationship
between the mechanism of this “blunted” TSH response and depression is unknown. Numerous
recent studies have characterized similarities and interactions between the immune
and neuroendocrine systems. As the immune system both produces and responds to TSH,
we utilized a peripheral blood leukocyte system to compare immunoreactive (ir)-TSH
responsiveness in 10 adult patients (1 man, 9 women) with Research Diagnostic Criteria
for major depressive disorder to that of 9 control subjects. All subjects had normal
baseline serum TSH and T4 concentrations. Isolated mononuclear leukocytes were treated
in vitro with either 0.5 μg/ml staphylococcal enterotoxin A (SEA), 50 μg/ ml TRH,
or no stimulant. After incubation, the cells were monitored for ir-TSH production
by indirect immunofluorescence and reverse hemolytic plaque assay using antisera to
TSH-β. The culture supernates were analyzed by TSH radioimmunoassay. SEA- and TRH-treated
cell cultures from depressed individuals had significantly fewer immunofluorescent
positive cells, as well as significantly fewer and smaller plaques, than did similarly
treated leukocytes from control subjects. The increase in supernatant ir-TSH was significantly
less in TRH-treated cultures from depressed patients as compared to normals (p < 0.05). These results suggest that examination of mononuciear leukocyte TSH production may
reflect an altered state of neuroendocrine function and may thus be a useful marker
for major depressive disorder.
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Article info
Publication history
Received in revised form:
September 17,
1987
Received:
July 7,
1987
Footnotes
☆Supported in part by the Office of Naval Research Grant N00014-84-K-0486, the George and Mary Josephine Hamman Foundation, the University of Texas Medical Branch Department of Psychiatry, and a Kempner Postdoctoral Fellowship to Deborah V. Harbour.
Identification
Copyright
© 1988 Published by Elsevier Inc.
