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By
From the * Division of Biology and Medicine, Brown University, Providence, Rhode Island 02912;
and Early infection with murine cytomegalovirus (MCMV) induces circulating levels of interleukin
(IL)-12, interferon (IFN)- Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine,
Atlanta, Georgia 30322
, and tumor necrosis factor (TNF). Studies presented here further characterize these responses by defining kinetics and extending evaluation to include IL-1, IL-6,
and glucocorticoids. IL-12 p40, IFN-, TNF, IL-1
, and IL-6 were shown to be increased,
but IL-1
was undetectable, in serum of MCMV-infected mice. The IL-12 p40, IFN-, TNF,
and IL-6 responses were dramatic with peak levels reaching >150-10,000 pg/ml at 32-40 h
after infection and rapidly declining thereafter. Glucocorticoid induction, peaking at 36 h and
reaching 30-fold increases above control values, accompanied the cytokine responses. Mice
with cytokine deficiencies or neutralized cytokine function demonstrated that IL-6 was the
pivotal mediator of the glucocorticoid response, with IL-1 contributing to IL-6 production.
The IL-6 requirement appeared to be specific for virus-type stimuli as the synthetic analogue of
viral nucleic acid, polyinosinic-polycytidylic acid, also induced IL-6-dependent glucocorticoid
release, but treatments with the bacterial product lipopolysaccharide and a non-immune physical
restraint stressor elicited IL-6-independent responses. Collectively, the results identify IL-6 as a
primary mediator of glucocorticoid induction, and elucidate specific pathways of interactions
between immune and neuroendocrine systems during viral infection.
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