ArticleBMC infectious diseases2025
Hypoxia-inducible factor-1α exacerbates immune injury induced by influenza A virus and Streptococcus pneumoniae coinfection.
Article in BMC infectious diseases, 2025. 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
backgroundInfluenza A virus (IAV) and Streptococcus pneumoniae (S. pneumoniae) coinfection during influenza pandemics is a significant contributor to mortality, mainly due to uncontrolled pathogen replication and an exaggerated immune response that often culminates in a cytokine storm. Hypoxia-inducible factor-1α (HIF-1α), a key regulator of cellular responses to hypoxia, has been implicated in various inflammatory processes; however, its role in pneumonia induced by IAV and S. pneumoniae coinfection remains unclear.
resultsIn this study, we established a model of IAV-S. pneumoniae coinfection and interfered with HIF-1α expression. The coinfection markedly increased both the expression and nuclear translocation of HIF-1α, which was accompanied by upregulated secretion of proinflammatory cytokines and exacerbated lung inflammation. Treatment with 2-ME2, a HIF-1α signaling inhibitor, attenuated the inflammatory responses in coinfection mice. Conversely, treatment with DMOG, a HIF-1α activator, exacerbated inflammation. Furthermore, we predicted downstream target genes of HIF-1α associated with infection and inflammatory responses, and validated the downregulation of a hub gene, Toll-like receptor 2 (TLR2), during IAV-S. pneumoniae coinfection.
conclusionOverall, this study demonstrates that upregulation of HIF-1α is strongly associated with severe inflammatory responses in IAV-S. pneumoniae coinfection, highlighting its potential as a therapeutic target for mitigating inflammation-related pathology in coinfected hosts. CLINICAL TRIAL NUMBER: Not applicable.
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