ReviewFrontiers in immunology2020
Cross-Talk Between Alveolar Macrophages and Lung Epithelial Cells is Essential to Maintain Lung Homeostasis.
Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
139 citing papers in PubMed, 238 citations in OpenAlex.
- Myeloid TLR2 signaling amplifies immunopathology in influenza-infected murine neonates.American journal of respiratory cell and molecular biology · 2026Article
- The Tie-2 agonist PMC-403 inhibits endothelial damage induced by e-cigarette vapor or LPS.Respiratory research · 2026Article
- Alveolar epithelial depletion of βPAK-interacting exchange factor drives spontaneous pulmonary fibrosis by impairing stemness.Signal transduction and targeted therapy · 2026Article
- Pulmonary Delivery of Self-Amplifying RNA: Balancing Inflammation and Durable Transgene Expression.ACS nano · 2026Article
- Homeostatic Regulation of Lung Dendritic Cells at Steady State.Immune network · 2026Review
- Piezo1-specific deletion in macrophage attenuates radiation-induced lung injury progression in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- The emerging regulatory roles of non-coding RNA in Ventilator-induced Lung Injury.Non-coding RNA research · 2026Review
- CQMUH-011 mitigated LPS-induced acute lung injury in neonatal rabbits.Scientific reports · 2026Article
- Breathing lung-on-chip: a versatile tool for assessing respiratory toxicity across multiple therapeutic modalities.Archives of toxicology · 2026Article
- Integrated bulk RNA-seq and scRNA-seq identification of a novel "PET-Translational cancer research · 2026Article
- M2 Macrophage-Derived Exosomes Ameliorate BPD by Inhibiting Ferroptosis via Suppression of the ZAKα-p38 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2026Article
- Live imaging of human airway epithelial repair in precision-cut lung slices after targeted cell damage.Biochemistry and biophysics reports · 2026Article
- Attenuation of canine distemper virus leads to a potent antiviral innate immune response with restricted infection of alveolar macrophages.Journal of virology · 2026Article
- Recent perspectives on macrophage memory: types, mechanisms, and characteristics in pulmonary diseases.Cell communication and signaling : CCS · 2026Review
- Role of connexin 43 in hyperoxia-induced bronchopulmonary dysplasia and associated pulmonary hypertension.PloS one · 2026Article
- Exploring the Mechanism of Therapeutic Effects of Polydatin in Lung Ischemia-Reperfusion Injury by Network Pharmacology and Experiment Validation.Journal of inflammation research · 2026Article
- Lung scRNA-seq reveals chronic inflammation and emphysemous phenotype in mice with osteogenesis imperfecta.Frontiers in genetics · 2026Article
- Gut microbiota in acute lung injury/acute respiratory distress syndrome: mechanistic insights and therapeutic opportunities via the gut-lung axis.Frontiers in cellular and infection microbiology · 2026Review
- Exosomal miR-2110 from PM2.5-Exposed Lung Epithelial Cells Targets SRSF1 to Promote M1 Macrophage Polarization and Inflammatory Responses in COPD.International journal of chronic obstructive pulmonary disease · 2026Article
- Respiratory epithelial cells as central mediators of immune crosstalk in SARS-CoV-2 infection.Frontiers in immunology · 2026Review
79 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
4 authors at 3 institutions in 2 countries.
Funding
Abstract
The main function of the lung is to perform gas exchange while maintaining lung homeostasis despite environmental pathogenic and non-pathogenic elements contained in inhaled air. Resident cells must keep lung homeostasis and eliminate pathogens by inducing protective immune response and silently remove innocuous particles. Which lung cell type is crucial for this function is still subject to debate, with reports favoring either alveolar macrophages (AMs) or lung epithelial cells (ECs) including airway and alveolar ECs. AMs are the main immune cells in the lung in steady-state and their function is mainly to dampen inflammatory responses. In addition, they phagocytose inhaled particles and apoptotic cells and can initiate and resolve inflammatory responses to pathogens. Although AMs release a plethora of mediators that modulate immune responses, ECs also play an essential role as they are more than just a physical barrier. They produce anti-microbial peptides and can secrete a variety of mediators that can modulate immune responses and AM functions. Furthermore, ECs can maintain AMs in a quiescent state by expressing anti-inflammatory membrane proteins such as CD200. Thus, AMs and ECs are both very important to maintain lung homeostasis and have to coordinate their action to protect the organism against infection. Thus, AMs and lung ECs communicate with each other using different mechanisms including mediators, membrane glycoproteins and their receptors, gap junction channels, and extracellular vesicles. This review will revisit characteristics and functions of AMs and lung ECs as well as different communication mechanisms these cells utilize to maintain lung immune balance and response to pathogens. A better understanding of the cross-talk between AMs and lung ECs may help develop new therapeutic strategies for lung pathogenesis.
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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.