ArticleProceedings of the National Academy of Sciences of the United States of America2015
Influenza viral neuraminidase primes bacterial coinfection through TGF-β-mediated expression of host cell receptors.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
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Who cites it
86 citing papers in PubMed.
- Blocking Extracellular Cyclophilin A-Mediated Adhesion Protects Against Bacterial Infection.MedComm · 2026Article
- Current insights into bacterial secondary infection following influenza A virus infection.Frontiers in microbiology · 2026Review
- Comparative progress on the mechanisms of airway mucosal injury induced by different pathogens: SARS-CoV-2, influenza A virus, and Mycoplasma pneumoniae.Frontiers in cellular and infection microbiology · 2026Review
- PRRSV promotes bacterial infection by remodeling actin cytoskeleton and cell membrane proteins.mBio · 2025Article
- Respiratory bacterial and viral pathogen spectrum among influenza-positive and influenza-negative patients.BMC infectious diseases · 2025Article
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- Orthogonal CRISPR/Cas system facilitated dual-color fluorescence fiber-embedded optofluidic nano-biochip for parallel amplification-free on-site detection of bacterium and virus.Mikrochimica acta · 2025Article
- The intricate interplay among microbiota, mucosal immunity, and viral infection in the respiratory tract.Journal of translational medicine · 2025Review
- Positive Regulation of Cellular Proteins by Influenza Virus for Productive Infection.International journal of molecular sciences · 2025Review
- Therapeutic potential of exosomal lncRNAs derived from stem cells in wound healing: focusing on mesenchymal stem cells.Stem cell research & therapy · 2025Review
- Understanding the Molecular Interactions Between Influenza A Virus andPathogens (Basel, Switzerland) · 2025Article
- Impact of the COVID-19 Pandemic on Epidemiological Trends in Pediatric Cervical Abscess-Forming Infections.Microorganisms · 2025Article
- Post-influenza bacterial infection: mechanisms of pathogenesis and advances in therapeutic strategies.Frontiers in microbiology · 2025Review
- The dynamic etiology and epidemiological patterns of acute respiratory tract infections during and post non-pharmacological interventions of SARS-CoV-2 in Shenzhen, China: a two years' prospective cohort study from June 2022.Frontiers in cellular and infection microbiology · 2025Article
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- Respiratory tract barrier dysfunction in viral-bacterial co-infection cases.The Japanese dental science review · 2024Review
- Glaesserella parasuis serotype 4 exploits fibronectin via RlpA for tracheal colonization following porcine circovirus type 2 infection.PLoS pathogens · 2024Article
- Airway epithelial CD47 plays a critical role in inducing influenza virus-mediated bacterial super-infection.Nature communications · 2024Article
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- The H9N2 avian influenza virus increases APEC adhesion to oviduct epithelia by viral NS1 protein-mediated activation of the TGF-β pathway.Journal of virology · 2024Article
26 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza infection predisposes the host to secondary bacterial pneumonia, which is a major cause of mortality during influenza epidemics. The molecular mechanisms underlying the bacterial coinfection remain elusive. Neuraminidase (NA) of influenza A virus (IAV) enhances bacterial adherence and also activates TGF-β. Because TGF-β can up-regulate host adhesion molecules such as fibronectin and integrins for bacterial binding, we hypothesized that activated TGF-β during IAV infection contributes to secondary bacterial infection by up-regulating these host adhesion molecules. Flow cytometric analyses of a human lung epithelial cell line indicated that the expression of fibronectin and α5 integrin was up-regulated after IAV infection or treatment with recombinant NA and was reversed through the inhibition of TGF-β signaling. IAV-promoted adherence of group A Streptococcus (GAS) and other coinfective pathogens that require fibronectin for binding was prevented significantly by the inhibition of TGF-β. However, IAV did not promote the adherence of Lactococcus lactis unless this bacterium expressed the fibronectin-binding protein of GAS. Mouse experiments showed that IAV infection enhanced GAS colonization in the lungs of wild-type animals but not in the lungs of mice deficient in TGF-β signaling. Taken together, these results reveal a previously unrecognized mechanism: IAV NA enhances the expression of cellular adhesins through the activation of TGF-β, leading to increased bacterial loading in the lungs. Our results suggest that TGF-β and cellular adhesins may be potential pharmaceutical targets for the prevention of coinfection.
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