ArticleThe Journal of clinical investigation2016
Macrophage-epithelial paracrine crosstalk inhibits lung edema clearance during influenza infection.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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
82 citing papers in PubMed, 115 citations in OpenAlex.
- CFTR in alveolar type 1 cells contributes to lung liquid secretion and host defense.JCI insight · 2026Article
- TNF superfamily member 14 drives post-influenza depletion of alveolar macrophages, enabling secondary pneumococcal pneumonia.The Journal of clinical investigation · 2026Article
- The ribosomal landscape in influenza A virus infection: from molecular mechanisms to clinical relevance.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Orchestrating immunopathology: the spectrum of programmed cell death pathways co-opted by influenza a virus in pulmonary immunity.Frontiers in immunology · 2026Review
- The role of Na,K‑ATPase in lung diseases (Review).Molecular medicine reports · 2025Review
- Sensing molecular carbon dioxide: a translational focus for respiratory disease.Physiological reviews · 2025Review
- Dissecting multilayer cell-cell communications with signaling feedback loops from spatial transcriptomics data.Genome research · 2025Article
- CFTR as a therapeutic target for severe lung infection.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- 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
- Viral infection induces inflammatory signals that coordinate YAP regulation of dysplastic cells in lung alveoli.The Journal of clinical investigation · 2024Article
- Cell-intrinsic regulation of phagocyte function by interferon lambda during pulmonary viral, bacterial super-infection.PLoS pathogens · 2024Article
- Cell Cross-Talk in Alveolar Microenvironment: From Lung Injury to Fibrosis.American journal of respiratory cell and molecular biology · 2024Review
- The guardians of pulmonary harmony: alveolar macrophages orchestrating the symphony of lung inflammation and tissue homeostasis.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Review
- Signaling pathways and potential therapeutic targets in acute respiratory distress syndrome (ARDS).Respiratory research · 2024Review
- Advances and Applications of Lung Organoids in the Research on Acute Respiratory Distress Syndrome (ARDS).Journal of clinical medicine · 2024Review
- Alveolar macrophage-expressed Plet1 is a driver of lung epithelial repair after viral pneumonia.Nature communications · 2024Article
- Exploring the host response in infected lung organoids using NanoString technology: A statistical analysis of gene expression data.PloS one · 2024Article
- The pathogenesis of influenza in intact alveoli: virion endocytosis and its effects on the lung's air-blood barrier.Frontiers in immunology · 2024Review
22 more citing papers are in PubMed but not listed here.
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Authors and funding
19 authors at 3 institutions in 3 countries.
Funding
Abstract
Influenza A viruses (IAV) can cause lung injury and acute respiratory distress syndrome (ARDS), which is characterized by accumulation of excessive fluid (edema) in the alveolar airspaces and leads to hypoxemia and death if not corrected. Clearance of excess edema fluid is driven mostly by the alveolar epithelial Na,K-ATPase and is crucial for survival of patients with ARDS. We therefore investigated whether IAV infection alters Na,K-ATPase expression and function in alveolar epithelial cells (AECs) and the ability of the lung to clear edema. IAV infection reduced Na,K-ATPase in the plasma membrane of human and murine AECs and in distal lung epithelium of infected mice. Moreover, induced Na,K-ATPase improved alveolar fluid clearance (AFC) in IAV-infected mice. We identified a paracrine cell communication network between infected and noninfected AECs and alveolar macrophages that leads to decreased alveolar epithelial Na,K-ATPase function and plasma membrane abundance and inhibition of AFC. We determined that the IAV-induced reduction of Na,K-ATPase is mediated by a host signaling pathway that involves epithelial type I IFN and an IFN-dependent elevation of macrophage TNF-related apoptosis-inducing ligand (TRAIL). Our data reveal that interruption of this cellular crosstalk improves edema resolution, which is of biologic and clinical importance to patients with IAV-induced lung injury.
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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.