ArticleJournal of microbiology (Seoul, Korea)2026
Vitamin D disrupts NS1-TUFM interaction to suppress pathogenic mitophagy in RSV-induced mitochondrial injury of bronchial epithelial cells.
Article in Journal of microbiology (Seoul, Korea), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
This study aims to examine the mechanism by which vitamin D mitigates bronchiolitis caused by respiratory syncytial virus (RSV) through the regulation of RSV nonstructural protein 1 (NS1)-TUFM-mediated mitophagy in bronchial epithelial cells. Clinical serum and PBMC samples from RSV-infected children and healthy controls were analyzed for vitamin D, mitochondrial DNA, mitophagy markers (LC3, ATG5, VDAC1, TOMM20, and COXIV), TUFM, and inflammatory cytokines (IL-6, IL-8, and TNF-α). In vitro, human bronchial epithelial cells Beas-2B were transfected with RSV-NS1 plasmid and TUFM silencing or overexpression constructs. Vitamin D (0.1-10 μM) was administered to evaluate mitophagy inhibition using Western blot, immunofluorescence, and JC-1 staining. NS1-TUFM interaction was confirmed by co-immunoprecipitation. RSV-positive patients exhibited reduced serum vitamin D, elevated TUFM and mitophagy markers, impaired mitochondrial mass, and increased inflammation. Vitamin D inversely correlated with LC3 and TUFM. RSV-NS1 overexpression induced mitochondrial translocation of NS1, TUFM-dependent mitophagy activation, and mitochondrial dysfunction (JC-1 depolarization). Vitamin D (10 μM) suppressed mitophagy by redistributing NS1 to the cytosol and reducing mitochondrial TUFM. TUFM overexpression abolished the protective effects of vitamin D on mitophagy and inflammation. In conclusion, vitamin D inhibits mitophagy in bronchial epithelial cells infected with RSV by disrupting NS1-TUFM interaction, suggesting that the vitamin D-TUFM axis may serve as a potential therapeutic target.
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