Gestational nicotine exposure alone or in combination with ethanol down-modulates offspring immune function

Prenatal nicotine exposure has been shown to disrupt the development of a n umber of peripheral organs. In the current study, we examined the effects o f gestational nicotine exposure, alone or in combination with ethanol expos ure, on offspring immune function. Timed pregnant rats were treated with ei ther nicotine (6 mg/kg/day) from gestation day 4-20 using subcutaneously im planted osmotic mini-pumps or ethanol administered in the drinking water (1 5% w/v) from gestation day 10-20. The combined exposure group received both treatments, The ability of offspring T and B cells to proliferate in respo nse to nonspecific stimulation by Concanavalin A or lipopolysaccharide, res pectively, was determined on postnatal days 9, 15, 22 29, 64. and 86. Offsp ring splenocyte beta(2)-adrenoceptor binding was also measured. Nicotine or nicotine + ethanol suppressed splenocyte responsiveness to Conc anavalin A or lipopolysaccharide which was similar in timing and magnitude to that seen with ethanol alone. Splenocytes from these groups remained sub responsive to stimulation well into adulthood. The combined drug treatment caused an overall reduction in spleen B-adrenergic receptor binding whereas the individual drug treatments did not alter the development of spleen bet a-adrenergic receptors. Our results indicate that prenatal nicotine exposure can cause long-term su ppression of the proliferative response of offspring immune cells. Moreover , the effects of nicotine + ethanol may cause more severe deficits in adult hood. (C) 2000 International Society for Immunopharmacology. Published by E lsevier Science Ltd. All rights reserved.