EFFECT OF NICOTINE ON THE IMMUNE-SYSTEM - POSSIBLE REGULATION OF IMMUNE-RESPONSES BY CENTRAL AND PERIPHERAL MECHANISMS

Nicotine (NT) treatment impairs T-cell receptor (TCR)-mediated signali ng, leading to the arrest of T cells in the G1 phase of the cell cycle and inhibition of the antibody plaque-forming cell (AFC) response to sheep red blood cells (SRBC). This paper summarizes some of the previo us findings related to cigarette smoke/NT and the immune response, and presents preliminary evidence suggesting that mice chronically treate d with NT (0.5 mg/day/kg body weight) have a depressed inflammatory re sponse in the turpentine-induced abscess model of inflammation. This a bility of nicotine to attenuate an inflammatory response may also be t he cause of reduced mortality of chronically nicotine-treated mice fro m acute influenza A pneumonitis. Moreover, in LEW rats, decreased anti -SRBC AFC responses were also observed after intracerebroventricular ( ICV) administration of relatively small concentrations of NT (28 mu g/ day/kg body weight) which, when given peripherally, did not affect the AFC response. In vitro the addition of NT to T cells increased protei n tyrosine kinase (PTK) activity and intracellular Ca2+ concentration [Ca2+](i). These results support the hypothesis that NT alters immune responses by directly interacting with T cells, as well as indirectly through brain-immune interactions. (C) 1998 Elsevier Science Ltd. All rights reserved.