ArticleJournal of translational medicine2025
FlaA N/C attenuates radiation-induced lung injury by promoting NAIP/NLRC4/ASC inflammasome autophagy and inhibiting pyroptosis.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Radiotherapy-Induced Side Effects: Epidemiology, Pathogenesis, Prevention and Treatments.MedComm · 2026Review
- Identification of PRKCB, NLRC4, and TNFSF10 as Key Regulators of the Lipid Metabolism-Autophagy Network in Atherosclerosis.Cell biochemistry and function · 2026Article
- Review
- Effects and potential mechanisms of the ultra-high dose rate radiotherapy on lung injury: a review.Radiation oncology (London, England) · 2025Review
- Chemokines as key mediators in RIPI: pathophysiology and translational potential.Frontiers in immunology · 2025Review
- New Exploration of Therapeutic Targets for Radiation Pneumonitis: Comparative Analysis of Molecular Pathways in Radiation-Induced and LPS-Induced Pneumonitis.International journal of medical sciences · 2025Review
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Authors and funding
11 authors.
Funding
Abstract
backgroundRadiation-induced lung injury (RILI) is the most common complication experienced by patients with thoracic tumors after radiotherapy. Among patients receiving thoracic tumor radiotherapy, 14.6-37.2% develop RILI. RILI is characterized by an acute inflammatory response; however, the exact mechanism remains unclear and an ideal drug is still lacking. In this study, we investigated the protective effects of flagellin A with linked C- and N-terminal ends (FlaA N/C) against the development of RILI.
methodsMice and bronchial epithelial cells were exposed to radiation (15 Gy) after FlaA N/C treatment. Lung injury, bronchial epithelial cell injury, and RILI were assessed by histological evaluation in vivo and cell viability and cell death detection in vitro. Pyroptosis was assessed by western blotting (WB), immunofluorescence (IF), and immunohistochemistry (IHC). To explore the molecular mechanisms by which FlaA N/C inhibits RILI, conditional Beclin 1 (Beclin1
resultsFlaA N/C attenuated radiation-induced lung tissue damage, pro-inflammatory cytokine release, and pyroptosis in vivo and cell viability, cell death, and pyroptosis in vitro. Mechanistically, FlaA N/C activated the neuronal apoptosis inhibitory protein (NAIP)/NLRC4/apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) inflammasome, which was then degraded during Beclin 1-mediated autophagy. Deletion of the FlaA N/C D0 domain reversed the inhibitory effect of FlaA N/C on radiation-induced pyroptosis in vivo and in vitro. Similarly, Nlrc4-knockout in vivo or inhibition of autophagy in vitro eliminated the protective effects of FlaA N/C against radiation-induced pyroptosis.
conclusionsThese results indicate that FlaA N/C attenuates RILI by promoting NAIP/NLRC4/ASC inflammasome autophagy and inhibiting pyroptosis. This study provides a potential approach for RILI intervention.
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