BMMSCs injected into the sulfur mustard-induced acute lung injury mouse model, the proportion of anti-inflammatory M2 macrophages was substantially increased, whereas that of M1 macrophages was decreased in BMMSCs-treated mice compared with the sulfur mustard group, and the expression of Toll-like receptor 4 (TLR4) greatly increased, that indicated BMMSCs can inhibit the differentiation of macrophages into pro-inflammatory M1 macrophages through the TRL4 signaling pathway and promote the differentiation of macrophages to anti-inflammatory M2 macrophages (Feng et al., 2019). Here, TLR4 is linked to injury.