Fig. 4

Activation of IL-17 signaling pathway is involved in PM-induced pulmonary fibrosis. A Venn diagram depicts the overlapping enriched KEGG pathways based on the DEGs identified in the cell clusters of neutrophils, monocytes and fibroblasts in control and PM exposure group by scRNA-seq. B IL-17 signaling pathway is emerged from analysis of enriched KEGG pathways among the respective DEGs in 10 cell clusters. C The mean daily PM2.5 concentration (μg/m³, as shown in left y-axis) and cumulative exposure burden in mouse lungs (μg, as shown in right y-axis) calculated by MMPD program. D IL-17A mRNA expression in lung tissue from control and PM exposed groups at T1 (11 d), T2 (15 d), T3 (23 d), 8-weeks (56 d) and 16-weeks (112 d), and the respective cumulative exposure burdens. Results were calculated as fold changes versus the corresponding control group (N = 5). The data are expressed as mean ± SD. **P < 0.01; ***P < 0.001 compared with PM-exposed mice at different time points. ^aP < 0.001 compared with control mice at T1; ^bP < 0.001 compared with control mice at T2; ^cP < 0.001 compared with control mice at T3; ^dP < 0.001 compared with control mice at 8 weeks; ^eP < 0.001 compared with control mice at 16 weeks. E Contents of IL-17A in lung tissue from WT and IL-17A^−/− mice in control and PM exposed group following 8-week and 16-week exposure (N = 5). The data are expressed as mean ± SD. NS: Not significant; *P < 0.05; **P < 0.01; ***P < 0.001 compared with the control mice. ^###P < 0.001 compared with the WT PM-exposed mice (IL-17A^−/−-PM vs WT-PM). Con: control group; Exp: PM exposure group; DEGs: differential expressed genes