Fetal/neonatal ethanol exposure irreversibly alters immune parameters in young mice (36.28)

Abstract

Abstract Chronic ethanol ingestion has been shown to impair immune defensive function of adult hosts to invading organisms. Children born to alcoholic mothers are known to have increased incidence and severity of infections, but EtOHÕs effect on the immune system in the fetus/neonate has not been well studied. We have developed a model of fetal/neonatal EtOH exposure in which female mice are maintained on 10% EtOH in the drinking water during breeding and gestation, and then on 12% EtOH during lactation. Pups have successfully been weaned and showed no significant difference in weights from controls through 42 days of age. These pups have been studied at 20 d (weaning) and 42 d (adolescence) for immunological cell numbers and function. Our data showed decreased splenic T and B cells in EtOH pups, but increased pulmonary leukocyte and dendritic cell (DC) numbers. Splenic DC and epidermal Langerhans cells numbers did not change. However, EtOH decreased baseline costimulatory molecule expression on splenic DC and the ability of these DC to stimulate allogeneic T cells, changes that persisted following cessation of EtOH exposure. These results indicate that mice born to EtOH-consuming mothers have immune deficiencies that are persistent following cessation of EtOH exposure. The dissection of T, B cell and DC dysfunction in EtOH pups is in progress.