IMMUNE AND ENDOCRINE REGULATION OF FOOD-INTAKE IN SICK ANIMALS

To understand why sick animals do not eat, investigators have studied how the immune system interacts with the central nervous system (CNS), where motivation to eat is ultimately controlled. The focus has been on the cytokines secreted by activated mononuclear myeloid cells, whic h include interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and tu mor necrosis factor-alpha (TNF-alpha). Either central or peripheral in jection of recombinant IL-1 beta, IL-6, and TNF-alpha reduce food-moti vated behavior and food intake in rodents. Moreover, these cytokines a nd their receptors are present in the endocrine system and brain, and antagonism of this system (i.e., the cytokine network) has been shown to block or abrogate anorexia induced by inflammatory stimuli. Recent studies indicate that the same cytokines act on adipocytes and induce secretion of leptin, a protein whose activity has been neuroanatomical ly mapped to brain areas involved in regulating food intake and energy expenditure. Therefore, many findings converge to suggest that the re duction of food intake in sick animals is mediated by inflammatory cyt okines, which convey a message from the immune system to the endocrine system and CNS. The nature of this interaction is the focus of this s hort review. (C) Elsevier Science Inc. 1998