Prolactin is secreted by the pituitary lactotropes under hypothalamic control by prolactin-inhibiting factors (predominantly dopamine) and to a lesser extent by prolactin-releasing factors (including thyrotropin-releasing hormone) (IhOID.§L§Llln§l 1992). In addition to its role in the induction of maternal lactogenesis, prolactin has other physiological functions including effects on the immune system ( Myrphy,etllla/ 1995).
Prolactin receptors are present on human T and B lymphocytes, and T lymphocytes depend on prolactin for maintenance of immune competence. In mice, inhibition of prolactin release results in impaired lymphocyte function, depressed lymphokine-dependent macrophage activation, and death from a normally non-lethal exposure to bacteria. Cyclosporin is known to compete with prolactin for a common binding site on T cells, and its immunosuppressive effect is thought to be exerted in part by blocking the prolactin receptor. Suppression of prolactin secretion by the dopamine agonist bromocriptine is emerging as an adjuvant immunosuppressive strategy in autoimmune disease and after organ transplantation.
Serum prolactin concentrations are assumed to rise in response to acute stress, possibly as part of a natural defense against infections. However, in chronic stress conditions prolactin levels are no longer elevated. In critically ill subjects, dopamine infusion induces severe hypoprolactinemia that has been linked with impaired
T-lymphocyte proliferative response (Devins, eLM 1992; Van d.en.B.ergM^^^ The lack of prolactin secretion during dopamine administration or prolonged stress may be a codeterminant of immune dysfunction (anergy) in the critically ill.
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