ArticleCell death & disease2025
Gasdermin E deficiency limits inflammation and lung damage during influenza virus infection.
Article in Cell death & disease, 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.
- Degradation of ACSL3 by influenza A virus shifts unfolded protein response from antiviral defense to viral evasion.Virologica Sinica · 2026Article
- L. AGILIS ALLEVIATES SALPINGITIS IN HENS Lactobacillus agilis alleviates salpingitis through the TLR4/MyD88/NF-κB pathway and gut microbiota interactions in aged laying hens.Poultry science · 2026Article
- Gasdermin E is dispensable for H1N1 influenza virus pathogenesis in mice.Microbiology spectrum · 2026Article
- Dissecting Cell Death Pathways in Influenza A Virus Infection: Comparative Insights from Human Models.Viruses · 2026Review
- Post-translational modification networks as master regulators of influenza virus replication, host adaptation, and immune evasion.Frontiers in immunology · 2026Review
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Authors and funding
10 authors.
Funding
Abstract
Severe influenza A virus (IAV) infections are associated with hyperinflammation and significant lung damage. Gasdermin E (GSDME) mediates pyroptosis, a lytic and inflammatory type of cell death. Cleavage of GSDME by caspase-3 releases the active N-terminal domain, which subsequently forms transmembrane pores, leading to cell lysis and death. In this study, we investigated a role for GSDME in severe influenza. Infection of human bronchial epithelial cells revealed that IAV induces GSDME cleavage and activation, with the magnitude and kinetics of GSDME activation differing between IAV strains. Caspase-3-mediated GSDME activation preceded and overwhelmed gasdermin D (GSDMD) activation. siRNA silencing in vitro confirmed both gasdermins are active in human bronchial epithelial cells and cooperate to drive IAV responses. IAV infection of mice promoted GSDME cleavage in E-cadherin
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