Maternal Stress Increases Risk of Allergic Lung Inflammation in Adult Mice

Abstract

Background: Allergies are increasing worldwide. The presence of atopic diseases inthe mother propagates the onset of allergic diseases in the offspring with aconsiderably stronger penetrance than atopic diseases of the father. Such observationchallenges genetic predispositions as the sole cause of allergic diseases.Epidemiological studies suggest that caregiver stress in the perinatal period maypredispose offspring to asthma. Only one group has studied the link between prenatalstress and neonatal asthma susceptibility in a murine model. Objectives: We aimed tostudy if the neonatal increased risk of developing allergic lung inflammation persistsafter puberty and if there are sex differences in susceptibility. Methods: PregnantBALB/c mice were subjected to a single restraint stress exposure at day 15 ofgestation. Pups were separated by gender and subjected to a well-known sub-optimalasthma model after puberty. Results: Adult mice born to stressed dams were moresusceptible to developing allergic pulmonary inflammation since an increase in thenumber of eosinophils in bronchoalveolar lavage (BAL), a greater peribronchial andperivascular infiltrate, a higher proportion of mucus-producing cells, and increased IL-4and IL-5 levels in BAL were detected compared to control mice. These effects weremore profound in females than males. Moreover, only females from stressed damsshowed an increase in IgE levels. Conclusions: Increased litter susceptibility to developallergic lung inflammation induced by maternal stress persists after puberty and ismore potent in females than in male mice.