ArticleAmerican journal of respiratory and critical care medicine2011
Fas determines differential fates of resident and recruited macrophages during resolution of acute lung injury.
Article in American journal of respiratory and critical care medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 219 papers, 1 of them a synthesis that pooled it.
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Who cites it
219 citing papers in PubMed, 1 synthesis or guideline pooled it, 333 citations in OpenAlex.
- Global Trends in Research of Macrophages Associated With Acute Lung Injury Over Past 10 Years: A Bibliometric Analysis.Frontiers in immunology · 2021Pooled it
- Monocytes in pneumonia: Functional plasticity and innate memory (Review).International journal of molecular medicine · 2026Review
- Alveolar macrophage-derived TGF-β promotes acute lung injury recovery by regulating inflammatory monocyte-derived macrophages.Journal of advanced research · 2026Article
- Article
- RNAseq analysis demonstrates polarization state-dependent responses to ambient particulate matter in a particle composition-specific manner.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Macrophage autophagy-dependent M2 polarization mediates the protective effect of ADSC-conditioned medium against acute lung injury.Stem cell research & therapy · 2026Article
- Recent perspectives on macrophage memory: types, mechanisms, and characteristics in pulmonary diseases.Cell communication and signaling : CCS · 2026Review
- Lineage tracing reveals the origins and dynamics of macrophages in lung injury and repair.Cell discovery · 2026Article
- Rab43 mitigates the inflammatory response in acute lung injury via MyD88 ubiquitination.Scientific reports · 2026Article
- Macrophage Phenotypic Plasticity and Inflammatory Mechanisms in Hyperoxia-Induced Lung Injury.Journal of inflammation research · 2026Review
- Divergent macrophage responses to Influenza A virus andFrontiers in immunology · 2026Article
- Association Between Ferritinophagy and M1 Macrophage Polarization During the Acute Phase of Childhood Allergic Asthma.Journal of inflammation research · 2026Article
- Neutrophil-macrophage crosstalk network in acute lung injury: feedback circuits linking cytokine storm and cell death.Frontiers in cellular and infection microbiology · 2026Review
- Alveolar dysregulation of host response in pneumonia and ARDS: implications for immune modulation and infection.Annals of intensive care · 2026Review
- Macrophage-specific therapy blocks the lung's mechanosensitive immune response to alveolar distension.JCI insight · 2025Article
- Review
- Siglec-F Protects Against Elastase-induced Lung Inflammation and Emphysema in Mice.bioRxiv : the preprint server for biology · 2025Article
- Centers for Medical Countermeasures against Radiation Consortium: Past, Present, and Beyond.Radiation research · 2025Review
- Short-Term Acid Sphingomyelinase Deficiency Exerts Proinflammatory and Antiapoptotic Effects during LPS-induced Lung Injury in Mice.American journal of respiratory cell and molecular biology · 2025Article
- Macrophages: Subtypes, Distribution, Polarization, Immunomodulatory Functions, and Therapeutics.MedComm · 2025Review
159 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
rationaleDuring acute lung injury (ALI) the macrophage pool expands markedly as inflammatory monocytes migrate from the circulation to the airspaces. As inflammation resolves, macrophage numbers return to preinjury levels and normal tissue structure and function are restored.
objectivesTo determine the fate of resident and recruited macrophages during the resolution of ALI in mice and to elucidate the mechanisms responsible for macrophage removal.
methodsALI was induced in mice using influenza A (H1N1; PR8) infection and LPS instillation. Dye labeling techniques, bone marrow transplantation, and surface immunophenotyping were used to distinguish resident and recruited macrophages during inflammation and to study the role of Fas in determining macrophage fate during resolving ALI. MEASUREMENTS AND MAIN
resultsDuring acute and resolving lung injury from influenza A and LPS, a high proportion of the original resident alveolar macrophages persisted. In contrast, recruited macrophages exhibited robust accumulation in early inflammation, followed by a progressive decline in their number. This decline was mediated by apoptosis with local phagocytic clearance. Recruited macrophages expressed high levels of the death receptor Fas and were rapidly depleted from the airspaces by Fas-activating antibodies. In contrast, macrophage depletion was inhibited in mice treated with Fas-blocking antibodies and in chimeras with Fas-deficient bone marrow. Caspase-8 inhibition prevented macrophage apoptosis and delayed the resolution of ALI.
conclusionsThese findings indicate that Fas-induced apoptosis of recruited macrophages is essential for complete resolution of ALI.
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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.