ArticlePLoS pathogens2017
Alveolar Macrophages Prevent Lethal Influenza Pneumonia By Inhibiting Infection Of Type-1 Alveolar Epithelial Cells.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.
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Who cites it
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 128 citations in OpenAlex.
- Prevalence of pneumonia and its associated factors among under-five children in East Africa: a systematic review and meta-analysis.BMC pediatrics · 2020Pooled it
- Leukotriene-modifying agent chemoprophylaxis for severe influenza illness: a multi-approach study.American journal of epidemiology · 2026Article
- Combating respiratory diseases with mucosal vaccines.Journal of virology · 2026Review
- Dying cells as architects of the stem cell niche: a conserved mechanism driving tissue regeneration and tumor therapy resistance.Cell communication and signaling : CCS · 2026Review
- TNF superfamily member 14 drives post-influenza depletion of alveolar macrophages, enabling secondary pneumococcal pneumonia.The Journal of clinical investigation · 2026Article
- Thyroid hormone receptor α signaling shapes innate and adaptive immune responses during viral infection.European thyroid journal · 2025Article
- Lung cell fates during influenza.Cell research · 2025Review
- Multilevel Analysis of Community Acquired Pneumonia Among 2-59 Months Old Children in Awi Zone, Northwest Ethiopia: A Community-Based Cross-Sectional Study.Health science reports · 2025Article
- Targeting alveolar macrophages: a promising intervention for pulmonary infection and acute lung injury.Cellular & molecular biology letters · 2025Review
- TLR7 deficiency enhances inflammation in the URT but reduces LRT immunity following influenza A infection.Scientific reports · 2025Article
- Risk factors for re-hospitalization within 90 days of discharge for severe influenza in children.BMC infectious diseases · 2025Article
- Alveolar Macrophages in Viral Respiratory Infections: Sentinels and Saboteurs of Lung Defense.International journal of molecular sciences · 2025Review
- The role of alveolar macrophages in viral respiratory infections and their therapeutic implications.Biochemistry and biophysics reports · 2024Review
- IFN-γ primes bone marrow neutrophils to acquire regulatory functions in severe viral respiratory infections.Science advances · 2024Article
- The deadly dance of alveolar macrophages and influenza virus.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Pregnancy enhances antiviral immunity independent of type I IFN but dependent on IL-17-producing γδScience advances · 2024Article
- Cell Cross-Talk in Alveolar Microenvironment: From Lung Injury to Fibrosis.American journal of respiratory cell and molecular biology · 2024Review
- Leptin Receptor Deficiency Impairs Lymph Node Development and Adaptive Immune Response.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Intestinal microbiota programming of alveolar macrophages influences severity of respiratory viral infection.Cell host & microbe · 2024Article
- Prevention of severe lung immunopathology associated with influenza infection through adeno-associated virus vector administration.Laboratory animal research · 2023Article
28 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The Influenza A virus (IAV) is a major human pathogen that produces significant morbidity and mortality. To explore the contribution of alveolar macrophages (AlvMΦs) in regulating the severity of IAV infection we employed a murine model in which the Core Binding Factor Beta gene is conditionally disrupted in myeloid cells. These mice exhibit a selective deficiency in AlvMΦs. Following IAV infection these AlvMΦ deficient mice developed severe diffuse alveolar damage, lethal respiratory compromise, and consequent lethality. Lethal injury in these mice resulted from increased infection of their Type-1 Alveolar Epithelial Cells (T1AECs) and the subsequent elimination of the infected T1AECs by the adaptive immune T cell response. Further analysis indicated AlvMΦ-mediated suppression of the cysteinyl leukotriene (cysLT) pathway genes in T1AECs in vivo and in vitro. Inhibition of the cysLT pathway enzymes in a T1AECs cell line reduced the susceptibility of T1AECs to IAV infection, suggesting that AlvMΦ-mediated suppression of this pathway contributes to the resistance of T1AECs to IAV infection. Furthermore, inhibition of the cysLT pathway enzymes, as well as blockade of the cysteinyl leukotriene receptors in the AlvMΦ deficient mice reduced the susceptibility of their T1AECs to IAV infection and protected these mice from lethal infection. These results suggest that AlvMΦs may utilize a previously unappreciated mechanism to protect T1AECs against IAV infection, and thereby reduce the severity of infection. The findings further suggest that the cysLT pathway and the receptors for cysLT metabolites represent potential therapeutic targets in severe IAV infection.
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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.