Maternal influences over offspring allergic responses

Abstract

Asthma occurs as a result of complex interactions of environmental and genetic factors. Clinical studies and animal models of asthma indicate offspring of allergic mothers have increased risk of development of allergies. Environmental factors including stress-induced corticosterone and vitamin E isoforms during pregnancy regulate the risk for offspring development of allergy. In this review, we discuss mechanisms for the development of allergic disease early in life, environmental factors that may impact the development of risk for allergic disease early in life, and how the variation in global prevalence of asthma may be explained, at least in part, by some environmental components.

Fig. 1

Model of maternal transmission of risk for allergy in offspring. Female mice are sensitized with chicken egg ovalbumin (OVA)/alum on weeks 1 and 2 and then challenging with OVA three times on weeks 4, 8, and 12 [–14]. After the last OVA challenge in week 12, these female mice are mated [–14]. To determine allergen responsiveness in the offspring, the offspring are treated with a suboptimal OVA protocol, such that the neonates receive only one instead of two OVA/alum treatments at postnatal day 3–5, and then starting 7 days later, the neonates are challenged with aerosolized OVA for three consecutive days [–14]. a Normal mothers. b Allergic mothers. c Dendritic cells are isolated from the spleens of pups from allergic mothers before pup treatment with allergen. These dendritic cells are transferred to pups from non-allergic mothers. d Macrophages are isolated from the spleens of pups from allergic mothers before pup treatment with allergen. Macrophages are transferred to pups from non-allergic mothers. e Allergic mothers are supplemented with α-tocopherol at the time of mating