Adolescent nicotine: deficits in immune function

Maternal cigarette smoking during pregnancy is known to alter immune functi on in the offspring and recent studies with animals indicate that prenatal nicotine exposure leads to lasting deficiencies in T-lymphocyte mitogenic r esponses, likely through excessive cholinergic stimulation during a critica l stage of development. The current study was conducted to determine if the vulnerable period for nicotine-induced mis-programming of immune responses extends into adolescence, the stage at which most smokers begin tobacco us e. Adolescent rats were given nicotine via osmotic minipump infusions on po stnatal days (PN) 30-47.5, using a regimen that produces plasma levels (25 ng/ml) of nicotine similar to those in smokers or in users of transdermal n icotine patches. Toward the end of the infusion period (PN45) and 1 month a fter termination of nicotine exposure (PN80), we examined the mitogenic res ponses of splenocytes to Concanavalin A. Although no deficiencies were seen on PN45, there were robust decreases in mitogenic responses on PN80, with deficits apparent at both suboptimal and optimal concentrations of Concanav alin A. These results indicate that the adolescent immune system is vulnera ble to nicotine-induced disruption of T-cell function. (C) 2001 Elsevier Sc ience B.V. All rights reserved.