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. 2022 Jan 31;12:824101. doi: 10.3389/fcimb.2022.824101

Figure 3.

Figure 3

Signaling pathways involved in mediating inflammatory responses are downregulated in co-infection compared to P. aeruginosa mono-infection in mouse PCLS. (A) 3D PCA plot of three independent experiments. Non-treated PCLS (Control) and PCLS infected with P. aeruginosa or S. mitis, or co-infected with both two bacteria (Co-infection) were lysed 8 h post infection for RNA isolation and expression profiling. (B–D, F) Volcano Plot of genes that are significantly different between the comparison “P. aeruginosa vs. Control” (B), “S. mitis vs. Control” (C), “S. mitis vs. P. aeruginosa(D), “Co_infection vs. P. aeruginosa(F). FC, fold change; Padj, p-value adjusted; NS, not significant. (E) Signaling pathway analysis was performed with genes downregulated in the comparison “S. mitis vs. P. aeruginosa” (fold change ≤−1.5 and p-value adjusted ≤0.05). Top 10 downregulated KEGG pathways are displayed. (G–I) Signaling pathway analysis was performed with genes downregulated in the comparison “Co_infection vs. P. aeruginosa” (fold change ≤−1.5 and p-value adjusted ≤0.05). (G) Top 10 downregulated KEGG pathways. (H) Heatmap of genes grouping into the KEGG pathway “mTOR signaling”. (I) Heatmap of genes grouping into the KEGG pathway “Neutrophil extracellular trap formation”. The genes shown in the heatmaps fulfill the criteria: fold change ≤−1.5 and p-value adjusted ≤0.05. Ctr, non-treated PCLS; Pae, P. aeruginosa mono-infected PCLS; Smi, S. mitis mono-infected PCLS; Col, P. aeruginosa and S. mitis co-infected PCLS.