ArticleFrontiers in immunology2023
Immune predisposition drives susceptibility to pneumococcal pneumonia after mild influenza A virus infection in mice.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Type I interferon signaling in hematopoietic cells impairs neutrophil antibacterial function in the middle ear during viral co-infection.Cell reports. Medicine · 2026Article
- PRRSV promotes bacterial infection by remodeling actin cytoskeleton and cell membrane proteins.mBio · 2025Article
- Type I Interferon Targets Alveolar Macrophages to Promote Bacterial Pneumonia after Viral Infection.American journal of respiratory cell and molecular biology · 2025Article
- The Role of TLR4 in Lung Epithelial Cell Injury Caused by Influenza Virus Combined withMicroorganisms · 2025Article
- Changes in children respiratory infections pre and post COVID-19 pandemic.Frontiers in cellular and infection microbiology · 2025Article
- Post-influenza bacterial infection: mechanisms of pathogenesis and advances in therapeutic strategies.Frontiers in microbiology · 2025Review
- Establishment of a humanized ST6GAL1 mouse model for influenza research.Animal models and experimental medicine · 2024Article
- Mathematical Modeling of the Lethal Synergism of Coinfecting Pathogens in Respiratory Viral Infections: A Review.Microorganisms · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Introduction: A frequent sequela of influenza A virus (IAV) infection is secondary bacterial pneumonia. Therefore, it is clinically important to understand the genetic predisposition to IAV and bacterial coinfection. Methods: BALB/c and C57BL/6 (B6) mice were infected with high or low-pathogenic IAV and Results: Low-virulent IAV X31 (H3N2) rendered B6 mice extremely susceptible to SPn superinfection, while BALB/c mice remained unaffected. X31 infection alone barely induces IFN-γresponse in two strains of mice; however, SPn superinfection significantly enhances IFN-γ production in the susceptible B6 mice. As a result, IFN-γ signaling inhibits neutrophil recruitment and bacterial clearance, leading to lethal X31/ Discussion: The results establish that type 1 immune predisposition plays a key role in lethal susceptibility of B6 mice to pneumococcal pneumonia after mild IAV infection.
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