ArticleNature communications2025
Staphylococcus aureus induces Gasdermin A-dependent keratinocyte pyroptosis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Coronavirus Nsp5‑mediated dual‑site cleavage of GSDMA modifies its antiviral and proinflammatory functions.PLoS pathogens · 2026Article
- Dynamic tethering of M protein drives pathological inflammation during group A Streptococcus infections.PLoS pathogens · 2026Article
- Differential pathogenic and commensal response ofJournal of bacteriology · 2026Article
- The molecular mechanisms of pyroptosis and its implications in tumor immunotherapy.Molecular cancer · 2026Review
- GSDMA deficiency impairs cutaneous squamous cell carcinoma growth.Frontiers in oncology · 2026Article
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Authors and funding
7 authors.
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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 pathogenicity, in contrast to the conventional regulation of other gasdermins, which have dedicated host cell pathways. Gasdermins abundant in other tissues may have similar functions in host defense for the threat assessment of a microbe.
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