Cytokines and endocrine function: an interaction between the immune and neuroendocrine systems

It is known that microbial infection, tissue damage, autoimmune processes and endotoxin shock are associated with a variety of endocrine and metabolic changes, such as the activation of the pituitary-adrenal system, alteration of serum thyroid hormone levels, inhibition of reproductive function and altered carbohydrate metabolism (Geelhoed & Chernow, 1985). These changes could be regarded as nonspecific responses of the body to stress, increased catabolism or impaired caloric intake, although the exact mechanisms causing such endocrine and metabolic abnormalities have not yet been clarified. Recent advances in the search for chemical mediators in the immune system have afforded a new insight into the interaction between the immune and neuroendocrine systems. In particular, chemical mediators produced by lymphocytes and monocytes, which were originally called lymphokines and monokines, respectively, are now known to be produced in a variety of tissues other than leucocytes and to have a broad spectrum of physiological or pathophysiological actions in addition to the regulation of the immune system. The more generic name, cytokine, has recently been used instead of lymphokine and monokine. Cytokines have been shown to affect both endocrine and metabolic functions and they are now regarded as important factors which intimately link the immune and neuroendocrine systems. The catalogue of cytokines is still expanding. It includes interleukin (1L)1 to 11, tumour necrosis factor (TNF)-a and fi , interferon (1FN)-a, p and 7, and colony stimulating factors. Among the cytokines, IL-1, IL-2, IL-6, TNF-a and INF-y are major mediators of inflammation (Dinarello, 1989; Kishimoto, 1989). The effects of all these cytokines on endocrine functions have not been fully studied but accumulating evidence suggests important roles of cytokines in