{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["LaRock DL"],"funding":["NCATS NIH HHS","NIAID NIH HHS","U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)","Burroughs Wellcome Fund (BWF)","Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de Recherche en Santé du Canada)"],"pagination":["10570"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12658218"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(1)"],"pubmed_abstract":["Staphylococcus aureus is a common colonizer of human skin, which, despite its ubiquitous nature, has a high virulence potential. Tolerating microbes in health but responding effectively to pathogens presents a challenge to the barrier tissues. Here, we examined the interaction of S. aureus with skin keratinocytes to study this early step of pathogenesis and pathogen discrimination. During infection, the S. aureus protease Staphopain A (ScpA) cleaves inert Gasdermin A (GSDMA). This releases an active N-terminal fragment similar to that formed by host protease regulators of other gasdermins family members. The resulting cell death by pyroptosis allows keratinocytes to deprive invasive S. aureus of an intracellular niche. These data support a model of GSDMA as an autonomous sensor of pathogen"],"journal":["Nature communications"],"pubmed_title":["Staphylococcus aureus induces Gasdermin A-dependent keratinocyte pyroptosis."],"pmcid":["PMC12658218"],"funding_grant_id":["AI153071","PJT-463397","AI158452","R01 AI139188","UL1 TR002378","R01 AI153071","R01 AI158452","AI139188","AI106699","T32 AI106699","R01 AI180089","Investigator in the Pathogenesis of Infectious Disease"],"pubmed_authors":["Sherman JD","Qu C","McGavin MJ","LaRock CN","Read TD","Ngai W","LaRock DL"],"additional_accession":[]},"is_claimable":false,"name":"Staphylococcus aureus induces Gasdermin A-dependent keratinocyte pyroptosis.","description":"Staphylococcus aureus is a common colonizer of human skin, which, despite its ubiquitous nature, has a high virulence potential. Tolerating microbes in health but responding effectively to pathogens presents a challenge to the barrier tissues. Here, we examined the interaction of S. aureus with skin keratinocytes to study this early step of pathogenesis and pathogen discrimination. During infection, the S. aureus protease Staphopain A (ScpA) cleaves inert Gasdermin A (GSDMA). This releases an active N-terminal fragment similar to that formed by host protease regulators of other gasdermins family members. The resulting cell death by pyroptosis allows keratinocytes to deprive invasive S. aureus of an intracellular niche. These data support a model of GSDMA as an autonomous sensor of pathogen","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Nov","modification":"2026-06-07T04:32:39.369Z","creation":"2026-06-07T03:06:51.167Z"},"accession":"S-EPMC12658218","cross_references":{"pubmed":["41298504"],"doi":["10.1038/s41467-025-65674-3"]}}