Effects of environmental tobacco smoke exposure on pulmonary immune response in infant monkeys

Exposure to environmental tobacco smoke (ETS) in early life has adverse effects on lung development and increases asthma incidence and susceptibility to infection. We have previously reported that perinatal and postnatal exposure to ETS in infant monkeys leads to an impaired T(H)1 immune response in peripheral blood.

Determine whether ETS exposure during the perinatal period alters pulmonary immune maturation in the neonatal lung.

Nonhuman primates were exposed to ETS from gestation day 50 to 13 months postnatal age (perinatal ETS) or from 6 to 13 months (postnatal ETS). Control animals were only exposed to filtered air. T(H)1 and T(H)2-related cytokines, chemokines, and their corresponding receptors as well as transcription factors were analyzed in lung tissues at 13 months.

Animals exposed to ETS beginning in utero exhibited more profound alterations in T(H)1 factors compared with animals exposed to ETS beginning at 6 months postnatal age. In perinatal ETS-exposed monkeys, mRNA for IFN-gamma, IL-2, IFN-gamma-inducible protein 10, monokine induced by IFN-gamma, IFN-gamma-inducible T-cell chemoattractant, CXC chemokine receptor 3, IL-12 bioactive p70 subunit, and T-bet were significantly downregulated, whereas in postnatal ETS-exposed monkeys, only IFN-gamma, CXC chemokine receptor 3, and IL-12p70 were significantly downregulated. ETS effects on T(H)2 factors were less apparent and more variable: mRNA for thymus and activation-regulated chemokine was increased, and IL-10 protein was reduced.

Environmental tobacco smoke exposure during early life enhances a local T(H)2 immunity by impairing normal pulmonary T(H)1 immune maturation. This effect was greater in animals beginning ETS exposure in utero.