Maternal Transmission of Resistance to Development of Allergic Airway Disease

Abstract

Parental phenotype is known to influence the inheritance of atopic diseases, such as allergic asthma, with a maternal history being a more significant risk factor for progeny than paternal history. We hypothesized that recall Th1- or Th2-type immune responses during pregnancy would result in transfer of maternal factors that would differentially impact development of immune responsiveness in offspring. Following weaning, susceptibility and severity of allergic airway disease (a murine model of human asthma) was evaluated in progeny, disease being elicited by immunization with OVA-Al(OH)3 and challenge with aerosolized OVA. We found that progeny of mothers with Th1-biased immunity to OVA subjected to recall aerosol challenge during pregnancy had reduced levels of Ag-specific IgE and airway eosinophilia compared with progeny of mothers with Th2-biased immunity to OVA or naive mothers. Interestingly, progeny of mothers with Th1-type immunity to a heterologous albumin, BSA, were not protected from developing OVA-induced allergic airway disease. These findings demonstrated that maternal transfer of protection from development of allergic airway disease to offspring in this model of maternal Th1-type immunity was Ag specific.

<i>Mycobacterium vaccae</i> Immunization to Pregnant BALB/c Mice Ameliorated Lung Histopathology and Bone Marrow Eosinophila in Ovalbumin Sensitized Offsprings

“…In a recent study maternal transfer of protection from development of allergic airway disease to offspring in a murine model of maternal Th1 type immunity was demonstrated to be ag-specific. This study also confirmed that the transfer of maternal factors would impact on the development of immune response in offspring [11]. It has been demonstrated that healthy non-atopic subjects have detectable allergen-specific T-reg cells mediating their function through IL-10 and/or TGF-β production, suggesting an important contribution of T-reg, Tr1-like cells to the immune regulation in allergy [31].…”

“…Epidemiological studies have highlighted maternal asthma as an additional risk factor for developing the disease during childhood [8]- [10]. Apparently greater influence of maternal versus paternal asthma supports the idea that, besides genes, maternal immune status including the allergic conditions may be more critical to transferring asthma risk [11]. It was suggested that maternal asthma had additional risk for offsprings for an originally sensitized allergen.…”

Protective Role of Passively Transferred Maternal Cytokines against Bordetella pertussis Infection in Newborn Piglets

“…Furthermore, several lines of evidence support the notion of fetal and newborn immune imprinting. In animal models, maternal Th1 type cytokines during gestation were shown to contribute to the reduction of experimental allergic airway disease in the newborn (20). Similarly, in humans, maternal exposure to Th1 type cytokines during gestation alleviates atopic sensitization of the offspring (21,22).…”

Fetal–Maternal Alignment of Regulatory T Cells Correlates with IL-10 and Bcl-2 Upregulation in Pregnancy

“…In the murine model, maternal Th1-type immunity during pregnancy was shown to decrease the risk of experimental allergic airway disease in the offspring (8). Transplacental passage of allergen specific IgG also protected against asthma in the offspring in an IFN-g-dependent manner (9).…”