[No authors listed]
Pulmonary epithelial barrier dysfunction is a critical pathological component of lung injury, caused primarily by impaired epithelial cell migration. Moreover, macrophageâepithelial interactions in pulmonary alveoli may either protect or damage epithelial barrier function. To investigate the effects of different macrophage subtypes, M1 and M2, on lipopolysaccharide (LPS)âinduced epithelial barrier dysfunction, M1 and M2 macrophages were used to treat LPSâinjured musculus lung epithelial cells (MLEâ12). Barrier function was evaluated by monitoring cell monolayer permeability, Tâcell immunoglobulin mucin 3 (Timâ3) small interfering RNA and antiâmouse Timâ3 antibody were used to knockdown or block endogenous Timâ3, to verify the role of the Timâ3 in macrophageâmediated barrier protection in LPSâinjured MLEâ12 cells. LY294002 was used to inhibit the activity of PI3K to verify the role of the PI3K/Akt signaling pathway in the restoration of epithelial cell. The present results revealed that coâculture of LPSâtreated epithelial MLEâ12 cells with M1 macrophages decreased cell migration and promoted permeability, whereas coâculture with M2 macrophages caused the opposite effects. It was determined that blocking Tâcell immunoglobulin mucin 3 (Timâ3) signaling in macrophages and PI3K/Akt signaling in epithelial cells eliminated the barrier protection supplied by M2 macrophages. Timâ3, which maintains macrophage M2 polarization, is a key component of the macrophageâmediated barrierârepair process, while M2 macrophages regulate PI3K/Akt signaling in epithelial cells, which in turn enhances pulmonary epithelial barrier function by restoring cell migration.
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