ArticlePLoS pathogens2014
Alveolar macrophages are essential for protection from respiratory failure and associated morbidity following influenza virus infection.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 221 papers.
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Who cites it
221 citing papers in PubMed, 328 citations in OpenAlex.
- AXL mediates influenza A virus entry and drives virus-induced inflammation.Emerging microbes & infections · 2026Article
- Alveolar Macrophages: Development, Respiratory Homeostasis, Signal Pathways, Diseases, and Therapeutic Opportunities.MedComm · 2026Review
- Alveolar macrophages undergo postnatal transition from a hyperphagocytic and proinflammatory profile to a tolerogenic profile.iScience · 2026Article
- Article
- Macrophages orchestrate antiviral defense and epithelial repair in a human iPSC-derived alveolar air-liquid interface.JCI insight · 2026Article
- TRIM5 integrates hypoglycemic stress and influenza infection.Nature communications · 2026Article
- GM-CSF orchestrates monocyte and granulocyte responses to Cryptococcus gattii.PLoS pathogens · 2026Article
- Attenuation of canine distemper virus leads to a potent antiviral innate immune response with restricted infection of alveolar macrophages.Journal of virology · 2026Article
- Breathing and burning: metabolic control of alveolar macrophages by intracellular bacterial pathogens.Frontiers in physiology · 2026Review
- Accumulation of Quinolinic Acid Modulates the Pulmonary Immune Response During Influenza Infection.International journal of tryptophan research : IJTR · 2026Article
- Neonatal CD19Frontiers in immunology · 2026Article
- Bioprinted Ventilated 3D Alveoliform Epithelial Sacculoids.Research square · 2025Article
- Review
- Article
- Targeting a macrophage stemness factor to mitigate diseases post respiratory viral infection.bioRxiv : the preprint server for biology · 2025Article
- Opposite Responses of Interferon and Proinflammatory Cytokines Induced by Human Metapneumovirus and Respiratory Syncytial Virus in Macrophages.Pathogens (Basel, Switzerland) · 2025Article
- RACK1 promotes the development and function of alveolar macrophages through directly binding to and stabilizing PPARγ.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Targeting alveolar macrophages: a promising intervention for pulmonary infection and acute lung injury.Cellular & molecular biology letters · 2025Review
- Dual roles of influenza B virus neuraminidase mRNA vaccine in enhancing cross-lineage protection by supplementing inactivated split vaccination.Journal of virology · 2025Article
- Alveolar and Bone Marrow-derived Macrophages Differ in Metabolism and Glutamine Utilization.American journal of respiratory cell and molecular biology · 2025Article
161 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alveolar macrophages (AM) are critical for defense against bacterial and fungal infections. However, a definitive role of AM in viral infections remains unclear. We here report that AM play a key role in survival to influenza and vaccinia virus infection by maintaining lung function and thereby protecting from asphyxiation. Absence of AM in GM-CSF-deficient (Csf2-/-) mice or selective AM depletion in wild-type mice resulted in impaired gas exchange and fatal hypoxia associated with severe morbidity to influenza virus infection, while viral clearance was affected moderately. Virus-induced morbidity was far more severe in Csf2-/- mice lacking AM, as compared to Batf3-deficient mice lacking CD8α+ and CD103+ DCs. Csf2-/- mice showed intact anti-viral CD8+ T cell responses despite slightly impaired CD103+ DC development. Importantly, selective reconstitution of AM development in Csf2rb-/- mice by neonatal transfer of wild-type AM progenitors prevented severe morbidity and mortality, demonstrating that absence of AM alone is responsible for disease severity in mice lacking GM-CSF or its receptor. In addition, CD11c-Cre/Ppargfl/fl mice with a defect in AM but normal adaptive immunity showed increased morbidity and lung failure to influenza virus. Taken together, our results suggest a superior role of AM compared to CD103+ DCs in protection from acute influenza and vaccinia virus infection-induced morbidity and mortality.
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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.