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. Author manuscript; available in PMC: 2023 Oct 19.
Published in final edited form as: Cell Rep. 2023 Aug 22;42(9):113024. doi: 10.1016/j.celrep.2023.113024

Figure 3. SE protease EcpA primarily drives early inflammation in epicutaneous mouse skin model.

Figure 3.

(A) PCA analysis of bulk RNA-seq data from murine dorsal skin treated with epicutaneous application of 1 × 107 CFU/cm2 of SE wild-type or mutant strains SE ΔpsmδΔhld, SEDecpA, or SE ΔpsmδΔhldΔecpA for 24 h (n = 3 per group).

(B) Kyoto Encyclopedia of Genes and Genomes enriched pathway analysis of SE WT versus control treated mouse skin at 24 h

(C–E) Volcano plots of log2fold changed genes (red) between SE WT and various knockout (KO) strains.

(F) qPCR analysis of up-regulated inflammatory genes in murine skin treated for 24 h with epicutaneous application of 1 × 107 CFU/cm2 of SE wild-type or mutant strains SE ΔpsmδΔhld, SE ΔecpA, or SE ΔpsmδΔhldΔecpA for 24 h (n = 6 per group). Results are representative of at least two independent experiments. Mean ± SEM and a non-parametric unpaired Kruskal-Wallis analysis was used to determine statistical significance: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.