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. Author manuscript; available in PMC: 2021 Apr 21.
Published in final edited form as: J Allergy Clin Immunol. 2020 Jul 4;147(3):955–966.e16. doi: 10.1016/j.jaci.2020.06.024

FIG 2.

FIG 2.

S epidermidis (SE) cysteine protease EcpA disrupts the skin barrier and degrades DSG-1 and LL-37. A and B, Representative pictures of the murine back skin treated with 106 CFUs/cm2 SA or SE isolates for 48 hours and TEWL measurements (n = 5). C and D, Representative pictures of the back skin after colonization with 103to 106 CFUs/cm2 SE 1457 WT for 48 hours and TEWL measurements (n = 4). E, TEWL measurements of AD mouse model back skin (Balb/c Flg−/− + ovalbumin [OVA]) colonized for 24 hours with live 106 CFUs/cm2 SE 1457 WT or SE 1457 ΔecpA (n = 5 or 6). F, Gram-positive bacteria staining (in purple) of skin sections from mice treated with either 106 CFUs/cm2 of SE 1457 WT or SE 1457 ΔecpA (n = 5). G and H, Assessment of C57BL/6 murine back skin and TEWL measurements after treatment with 2.5 μg/cm2 of EcpA or vehicle for 24 hours (n = 3). I and J, Differentiated NHEKs were treated for 20 hours with 2.5 μg/mL of EcpA ± 20 μg/mL of cycloheximide (protein synthesis inhibitor). Immunoblotting for DSG-1, involucrin (IVL), corneodesmosin (CDSN), and β-actin. Quantification of DSG-1 was normalized on β-actin (n = 3) (see Table E4). K and L, Coomassie blue staining of in vitro proteolysis of LL-37 by EcpA and S aureus (strain 113) growth inhibition assay (n = 3). All data are representative of at least 2 independent experiments, and results are means ± SEMs. One-way ANOVAs (B, D, and E), Student t tests (H and J), and 2-way ANOVA (L) were used to determine statistical significance: *P < .05; **P < .01; ***P < .001, ****P < .0001. Ctl, Control.