biostudies-literatureYang CHHS | National Institutes of HealthHHS | National Institutes of Health (NIH)Cystic Fibrosis FoundationNIAID NIH HHSNCI NIH HHSCystic Fibrosis Foundation (CFF)e0013324https://www.ebi.ac.uk/biostudies/studies/S-EPMC11320951biostudies-literatureUnknown92(8)<i>Staphylococcus aureus</i> α-hemolysin (Hla) is a pore-forming toxin critical for the pathogenesis of skin and soft tissue infections, which causes the pathognomonic lesion of cutaneous necrosis (dermonecrosis) in mouse models. To determine the mechanism by which dermonecrosis develops during <i>S. aureus</i> skin infection, mice were given control serum, Hla-neutralizing antiserum, or an inhibitor of Hla receptor [A-disintegrin and metalloprotease 10 (ADAM10) inhibitor] followed by subcutaneous infection by <i>S. aureus,</i> and the lesions were evaluated using immunohistochemistry and immunofluorescence. Hla induced apoptosis in the vascular endothelium at 6 hours post-infection (hpi), followed by apoptosis in keratinocytes at 24 hpi. The loss of vascular endothelial (VE)-cadherin exprInfection and immunityα-Hemolysin-mediated endothelial injury contributes to the development of <i>Staphylococcus aureus</i>-induced dermonecrosis.PMC11320951P30 CA016058PARTID18P0R01 AI125489R01-AI125489Robledo-Avila FHPartida-Sanchez SMontgomery CPYang Cfalseα-Hemolysin-mediated endothelial injury contributes to the development of <i>Staphylococcus aureus</i>-induced dermonecrosis.<i>Staphylococcus aureus</i> α-hemolysin (Hla) is a pore-forming toxin critical for the pathogenesis of skin and soft tissue infections, which causes the pathognomonic lesion of cutaneous necrosis (dermonecrosis) in mouse models. To determine the mechanism by which dermonecrosis develops during <i>S. aureus</i> skin infection, mice were given control serum, Hla-neutralizing antiserum, or an inhibitor of Hla receptor [A-disintegrin and metalloprotease 10 (ADAM10) inhibitor] followed by subcutaneous infection by <i>S. aureus,</i> and the lesions were evaluated using immunohistochemistry and immunofluorescence. Hla induced apoptosis in the vascular endothelium at 6 hours post-infection (hpi), followed by apoptosis in keratinocytes at 24 hpi. The loss of vascular endothelial (VE)-cadherin expr2024-01-01T00:00:00Z2024 Aug2025-04-04T21:49:20.255Z2025-04-04T21:49:20.255ZS-EPMC113209513895366810.1128/iai.00133-24