Soothing signals: transplacental transmission of resistance to asthma and allergy

Abstract

The progressive rise in the prevalence of allergic diseases since the 1970s is widely attributed to diminished exposure to microbial stimuli, resulting in dysregulated immune functions during early life. Most studies investigating the mechanism behind this phenomenon have focused on postnatal microbial exposure. But emerging evidence suggests that such programming may also occur in the developing fetus as a result of microbial stimulation of the pregnant mother.

Figure 1.

Proposed mechanisms by which maternal exposure to bacteria protects against allergies in offspring. Aerosol exposure to microbe-containing dust particles induces mild-to-moderate inflammation in the lungs, including increased expression of TLRs and production of cytokines. Cytokines might then enter the bloodstream and be delivered directly to the placental tissues, where they depress TLR expression, cytokine production, and influence resident myeloid cell functions. Circulating cytokines might also enter the maternal bone marrow, where they stimulate and “program” myeloid precursor cells. Programmed DCs and monocytes could then enter the circulation, and some of these cells could traffic to the decidua, where they could replace resident myeloid populations and influence the local inflammatory milieu.