Alex Lindgren

During pregnancy it has been established that maternal immune cells can cross the placental barrier and take up residence in fetal tissues in a process called maternal microchimerism. These microchimeric cells are thought to help protect the fetus from infection, promote immune tolerance, and aid in fetal immune development. However, the mechanisms behind this transfer as well as the specific destinations and functions of these cells in fetal tissues are not well understood, in part due to the scarcity of these cells in conventionally-housed special pathogen free (SPF) mice. Recently, we have shown that natural microbial exposure (NME), in which laboratory mice are co-housed with pet-store mice, has profound effects on the immune cell composition, but it is unknown how microbial exposure affects microchimerism. In this experiment, we used SPF and NME mouse models to simulate varying microbial burdens. Fetal samples were collected at 17.5 days gestation from immunological centers (thymus, bone marrow, spleen, and liver). Flow cytometry was used to identify immune cell types (T cells, B cells, macrophages, NK cells, and neutrophils) and distinguish between maternal and fetal cell origins. Our results showed that higher microbial exposure increased maternal cell presence in fetal tissues across immune cell subsets and various tissues. This suggests that increased microbial exposure may enhance maternal cell transfer to the fetus, potentially supporting immune development and tolerance mechanisms crucial for infection resistance in the offspring and pregnancy success. Additionally, since the NME model showed higher levels of microchimerism, it is a more representative model for human pregnancy and a better model for studying microchimeric cells. Future studies could explore the function of these cells in fetal tissues and investigate whether fetal microchimerism (the transfer of fetal cells to the mother) is similarly influenced by microbial exposure.