Maternal smoking is associated with impaired neonatal Toll-like receptor (TLR) mediated immune responses

¹ School of Paediatrics and Child Health Research, University of Western Australia

^* To whom correspondence should be addressed. E-mail: susanp{at}ichr.uwa.edu.au.

	Abstract

Infants of smokers have much higher rates of respiratory infection, asthma and airway disease. In this study we assessed the effects of maternal smoking in pregnancy on neonatal Toll-like receptor (TLR) mediated immune responses as a possible contributing factor.

In a prospective birth cohort, we compared the cord blood immune responses of neonates of smoking and non-smoking mothers. Maternal and cord serum cotinine were measured to confirm the level of cigarette smoke exposure. Neonatal cytokine responses were assessed to optimal doses of TLR2, TLR3, TLR4 and TLR9 ligands.

Cotinine levels confirmed maternal reporting of cigarette smoking in pregnancy, with significantly higher cotinine levels in maternal and cord blood compared to the non-smoking group. Infants of smoking mothers showed significantly attenuated innate TLR-mediated responses compared to infants of non-smokers.

These findings show that in addition to effects on developing airways, maternal smoking also has significant immunologic effects in pregnancy that could contribute to the well recognised subsequent increased risk of respiratory infections and asthma. These effects appear to be mediated through effects on TLR-mediated innate response pathways that also promote regulatory pathways in the inhibition of allergic immune responses in the postnatal period, suggesting that other environmental interactions are highly relevant to the "hygiene hypothesis".

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