Fig. 2

Early effects of mesenchymal stem cells (MSCs) on oxygenation, lung edema, and alveolar inflammatory cells in acid aspiration acute lung injury. Wild-type MSCs ameliorated arterial oxygen tension (a) and alveolar–arterial oxygen gradient (b) in experimental model of acid aspiration lung injury in 24 h, as well as PTX3-deficient MSCs, albeit to a lesser extent (Kruskal–Wallis p < 0.05 [A] and p = 0.001 [B]; Dunn’s post hoc *p < 0.05 and **p < 0.01 vs. PBS. PBS n = 21; WT-MSCs n = 28; PTX3^−/−-MSCs n = 11). Total cell count (c) and total neutrophil (PMN) count (d) in the broncho-alveolar lavage (BAL) were decreased by WT-MSCs but not by PTX3^−/−-MSCs in experimental groups in 24 h (Kruskal–Wallis p < 0.05 [C] and p = 0.01 [D]; Dunn’s post hoc *p < 0.05 and **p < 0.01 vs. PBS. PBS n = 21; WT-MSCs n = 17; PTX3^−/−-MSCs n = 9). WT-MSCs significantly reduced lung edema (c), as measured by wet-to-dry lung weight ratio (wet/dry) in the experimental groups in 24 h (ANOVA p < 0.05 [e]; *Dunnett’s post hoc p < 0.05 vs. PBS. PBS n = 21; WT-MSCs n = 18; PTX3^−/−-MSCs n = 10). No difference was seen in BAL total protein concentrations (f) (PBS n = 22; WT-MSCs n = 20; PTX3^−/−-MSCs n = 10). (PBS = acid aspiration acute lung injury + intraperitoneal (i.p.) PBS treatment in 1 h; WT-MSCs = acid aspiration acute lung injury + i.p. wild-type MSCs treatment in 1 h; PTX3^−/−-MSCs = acid aspiration acute lung injury + i.p. PTX3-deficient MSCs treatment in 1 h)