Maternal Cigarette Smoke Exposure in mice induces a Th2-biased immune response in Offspring

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 intranasally challenged with house dust mite extract (HDM) to measure lung function, T cell subsets in the lungs, bronchoalveolar lavage fluid (BALF) cell counts, and antigen-specific serum immunoglobulins (IgE and IgG1) or were twice injected with Influvac vaccine to assess delayed-type hypersensitivity (DTH) response, serum IgG1 and IgG2a, and splenic T cells. 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. There was no discernible effect of maternal CS exposure on Th1 cell frequency in the lung of HDM-challenged offspring. HDM-sensitized and challenged offspring of air-exposed dams showed increased numbers of eosinophils in BALF, while maternal CS exposure further enhanced this inflammatory response in the 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.