ArticlePloS one2012
Poly I:C enhances susceptibility to secondary pulmonary infections by gram-positive bacteria.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
53 citing papers in PubMed, 79 citations in OpenAlex.
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- Microbiome-host interactions in the pathogenesis of acute exacerbation of chronic obstructive pulmonary disease.Frontiers in cellular and infection microbiology · 2024Article
- TLR7 promotes smoke-induced experimental lung damage through the activity of mast cell tryptase.Nature communications · 2023Article
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- Suppressing fatty acid synthase by type I interferon and chemical inhibitors as a broad spectrum anti-viral strategy against SARS-CoV-2.Acta pharmaceutica Sinica. B · 2022Article
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- Babaodan controls excessive immune responses and may represent a cytokine-targeted agent suitable for COVID-19 treatment.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Article
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- Dynamic Pneumococcal Genetic Adaptations Support Bacterial Growth and Inflammation during Coinfection with Influenza.Infection and immunity · 2021Article
- Pneumococcal carriage in children with COVID-19.Human vaccines & immunotherapeutics · 2021Article
- Altered Signal Transduction in the Immune Response to Influenza Virus andInternational journal of molecular sciences · 2021Review
- Childhood asthma heterogeneity at the era of precision medicine: Modulating the immune response or the microbiota for the management of asthma attack.Biochemical pharmacology · 2020Review
- RIG-I and TLR4 responses and adverse outcomes in pediatric influenza-related critical illness.The Journal of allergy and clinical immunology · 2020Observational
- Unique Roles forFrontiers in immunology · 2020Article
- The Impact of Type 1 Interferons on Alveolar Macrophage Tolerance and Implications for Host Susceptibility to Secondary Bacterial Pneumonia.Frontiers in immunology · 2020Review
- Respiratory Barrier as a Safeguard and Regulator of Defense Against Influenza A Virus andFrontiers in immunology · 2020Review
- Inflammation and Pneumonia: Why Are Some More Susceptible than Others?Clinics in chest medicine · 2018Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Secondary bacterial pneumonias are a frequent complication of influenza and other respiratory viral infections, but the mechanisms underlying viral-induced susceptibility to bacterial infections are poorly understood. In particular, it is unclear whether the host's response against the viral infection, independent of the injury caused by the virus, results in impairment of antibacterial host defense. Here, we sought to determine whether the induction of an "antiviral" immune state using various viral recognition receptor ligands was sufficient to result in decreased ability to combat common bacterial pathogens of the lung. Using a mouse model, animals were administered polyinosine-polycytidylic acid (poly I:C) or Toll-like 7 ligand (imiquimod or gardiquimod) intranasally, followed by intratracheal challenge with Streptococcus pneumoniae. We found that animals pre-exposed to poly I:C displayed impaired bacterial clearance and increased mortality. Poly I:C-exposed animals also had decreased ability to clear methicillin-resistant Staphylococcus aureus. Furthermore, we showed that activation of Toll-like receptor (TLR)3 and Retinoic acid inducible gene (RIG-I)/Cardif pathways, which recognize viral nucleic acids in the form of dsRNA, both contribute to poly I:C mediated impairment of bacterial clearance. Finally, we determined that poly I:C administration resulted in significant induction of type I interferons (IFNs), whereas the elimination of type I IFN signaling improved clearance and survival following secondary bacterial pneumonia. Collectively, these results indicate that in the lung, poly I:C administration is sufficient to impair pulmonary host defense against clinically important gram-positive bacterial pathogens, which appears to be mediated by type I IFNs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.