Prenatal maternal infection promotes tissue-specific immunity and inflammation in offspring

The immune system has evolved in the face of microbial exposure. How maternal infection experienced at distinct developmental stages shapes the offspring immune system remains poorly understood. Here, we show that during pregnancy, maternally restricted infection can have permanent and tissue-specific impacts on offspring immunity. Mechanistically, maternal interleukin-6 produced in response to infection can directly impose epigenetic changes on fetal intestinal epithelial stem cells, leading to long-lasting impacts on intestinal immune homeostasis. As a result, offspring of previously infected dams develop enhanced protective immunity to gut infection and increased inflammation in the context of colitis. Thus, maternal infection can be coopted by the fetus to promote long-term, tissue-specific fitness, a phenomenon that may come at the cost of predisposition to inflammatory disorders.

Automated summary

Research suggests that maternal restricted infection during pregnancy can have permanent and tissue-specific impacts on offspring immunity, with maternal interleukin-6 playing a key role in this process. This may indicate that maternal infection can affect fetal intestinal immune homeostasis, leading to altered inflammatory immune responses in offspring.