ArticleJournal of immunology (Baltimore, Md. : 1950)2018
Effects of Influenza on Alveolar Macrophage Viability Are Dependent on Mouse Genetic Strain.
Article in Journal of immunology (Baltimore, Md. : 1950), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 84 citations in OpenAlex.
- AXL mediates influenza A virus entry and drives virus-induced inflammation.Emerging microbes & infections · 2026Article
- Monocytes in pneumonia: Functional plasticity and innate memory (Review).International journal of molecular medicine · 2026Review
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- Biological sex influences immune response to influenza infection in juvenile outbred mice.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Macrophage Immune Responses in Viral Infections: Functional Plasticity and Therapeutic Targeting.Journal of microbiology and biotechnology · 2026Review
- Disease modulation by TIV vaccination during secondary pneumococcal infections in influenza-infected mice.Journal of virology · 2026Article
- TNF superfamily member 14 drives post-influenza depletion of alveolar macrophages, enabling secondary pneumococcal pneumonia.The Journal of clinical investigation · 2026Article
- Segmented filamentous bacteria reprogramming of alveolar macrophages limits postinfluenza bacterial pneumonia.Science immunology · 2026Article
- SARS-CoV-2-International journal of microbiology · 2026Review
- Emerging highly pathogenic H5N1 influenza triggers fibrotic remodeling in human airway organoids.Emerging microbes & infections · 2025Article
- Transient lung eosinophilia during breakthrough influenza infection in vaccinated mice is associated with protective and balanced Type 1/2 immune responses.Journal of virology · 2025Article
- Disease modulation by TIV vaccination during secondary pneumococcal infections in influenza-infected mice.bioRxiv : the preprint server for biology · 2025Article
- Omadacycline exhibits anti-inflammatory properties and improves survival in a murine model of post-influenza MRSA pneumonia.Antimicrobial agents and chemotherapy · 2025Article
- Type I Interferon Targets Alveolar Macrophages to Promote Bacterial Pneumonia after Viral Infection.American journal of respiratory cell and molecular biology · 2025Article
- Swine influenza A virus infection sets the local immunological landscape in subsequent infection with porcine reproductive and respiratory syndrome virus.Veterinary research · 2025Article
- The role of alveolar macrophages in viral respiratory infections and their therapeutic implications.Biochemistry and biophysics reports · 2024Review
- Dual therapy with corticosteroid ablates the beneficial effect of DP2 antagonism in chronic experimental asthma.Nature communications · 2024Article
- Damping excessive viral-induced IFN-γ rescues the impaired anti-Aspergillus host immune response in influenza-associated pulmonary aspergillosis.EBioMedicine · 2024Article
- The deadly dance of alveolar macrophages and influenza virus.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Predictive signature of murine and human host response to typical and atypical pneumonia.BMJ open respiratory research · 2024Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Secondary bacterial coinfections following influenza virus pose a serious threat to human health. Therefore, it is of significant clinical relevance to understand the immunological causes of this increased susceptibility. Influenza-induced alterations in alveolar macrophages (AMs) have been shown to be a major underlying cause of the increased susceptibility to bacterial superinfection. However, the mechanisms responsible for this remain under debate, specifically in terms of whether AMs are depleted in response to influenza infection or are maintained postinfection, but with disrupted phagocytic activity. The data presented in this article resolves this issue by showing that either mechanism can differentially occur in individual mouse strains. BALB/c mice exhibited a dramatic IFN-γ-dependent reduction in levels of AMs following infection with influenza A, whereas AM levels in C57BL/6 mice were maintained throughout the course of influenza infection, although the cells displayed an altered phenotype, namely an upregulation in CD11b expression. These strain differences were observed regardless of whether infection was performed with low or high doses of influenza virus. Furthermore, infection with either the H1N1 A/California/04/2009 (CA04) or H1N1 A/PR8/1934 (PR8) virus strain yielded similar results. Regardless of AM viability, both BALB/c and C57BL/6 mice showed a high level of susceptibility to postinfluenza bacterial infection. These findings resolve the apparent inconsistencies in the literature, identify mouse strain-dependent differences in the AM response to influenza infection, and ultimately may facilitate translation of the mouse model to clinical application.
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