M1-like, but not M0-or M2-like, macrophages, reduce RSV infection of primary bronchial epithelial cells in a media-dependent fashion

Respiratory syncytial virus (RSV) is a common childhood infection that in young infants can progress into severe bronchiolitis and pneumonia. Disease pathogenesis results from both viral mediated and host immune processes of which alveolar macrophages play an important part. Here, we investigated the role of different types of alveolar macrophages on RSV infection using an in vitro co-culture model involving primary tissue-derived human bronchial epithelial cells (HBECs) and human blood monocyte-derived M0-like, M1-like, or M2-like macrophages. It was hypothesized that the in vitro model would recapitulate previous in vivo findings of a protective effect of macrophages against RSV infection. It was found that macrophages maintained their phenotype for the 72-hour co-culture time period and the bronchial epithelial cells were unaffected by the macrophage media. HBEC infection with RSV was decreased by M1-like macrophages but enhanced by M0- or M2-like macrophages. The medium used during the co-culture also impacted the outcome of the infection. This work demonstrates that alveolar macrophage phenotypes may have differential roles during epithelial RSV infection, and demonstrates that an in vitro co-culture model could be used to further investigate the roles of macrophages during bronchial viral infection.

Automated summary

The study investigated the role of different types of alveolar macrophages in respiratory syncytial virus (RSV) infection using an in vitro co-culture model. The results showed that M1-like macrophages decreased HBEC infection with RSV, while M0- or M2-like macrophages enhanced the infection. The study also demonstrated the potential of the in vitro co-culture model to further investigate the roles of macrophages in bronchial viral infection.