Maternal cigarette smoke exposure in mice induces a Th2-biased immune response in offspring

Environmental cigarette smoke (CS) exposure have adverse health impacts that start during early pregnancy and persist throughout childhood and adolescence. Considering the pivotal role of immune development in early life, the present study investigated the effects of maternal CS exposure on allergy development and vaccine responsiveness in the offspring. Pregnant dams were exposed to either CS or air during pregnancy and lactation. Two weeks after weaning, the offspring were either challenged with HDM or were injected with Influvac vaccine. After the HDM challenges, lung function, T cells in the lungs, BALF cell counts, and serum immunoglobulins were assessed, while following vaccination, DTH response, serum immunoglobulins, and splenic T cells were measured. Lung resistance and antigen-specific serum IgE and IgG1 were significantly higher in HDM-sensitized and challenged offspring of CS-exposed dams compared to HDM-challenged offspring born to air-exposed dams. HDM-sensitized and challenged offspring of CS-exposed dams showed increased eosinophil counts in BALF. There was no discernible effect of maternal CS exposure on Th1 cell frequency in the lung of HDM-challenged offspring. Vaccinated offspring from both air- or CS-exposed dams exhibited a similar pattern in DTH response and IgG1 and IgG2a levels. However, maternal CS exposure resulted in higher splenic Th2 cell activation in vaccinated offspring compared to PBS-treated offspring. In conclusion, early life exposure to CS can affect immune development in offspring. The offspring showed a bias towards Th2 immunity resulting in an exacerbated allergic immune response to allergens.