ArticleFrontiers in immunology2024
Monocyte-derived alveolar macrophages are key drivers of smoke-induced lung inflammation and tissue remodeling.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 33 citations in OpenAlex.
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
- Spatial immune profiling of local tissues and its correlation with peripheral blood cytokines in lung squamous cell carcinoma patients with immune-related pneumonitis.Translational cancer research · 2026Article
- Regenerative therapeutics for chronic obstructive pulmonary disease.Pharmacological reviews · 2026Review
- Cigarette Smoke Induces the Pro-inflammatory Response of Lung Macrophages via Activation of the IL-33/ST2-Dependent Pathway.Immune network · 2026Article
- Spontaneous Pregravid Obesity Reshapes Fetal Immune Ontogeny in a Nonhuman Primate Model.bioRxiv : the preprint server for biology · 2026Article
- Airway injury induces alveolar epithelial responses mediated by macrophages.Cell reports · 2026Article
- Cigarette and Electronic Cigarette Exposure in Osteoarthritis: Immune Dysregulation and Inflammatory Signaling Pathways.International journal of general medicine · 2026Article
- Trained immunity and related memory responses in lung health and disease.Frontiers in immunology · 2026Review
- Association Between Monocyte-to-High Density Lipoprotein-Cholesterol Ratio and COPD Among US Adults: Findings from NHANES 1999-2018.International journal of chronic obstructive pulmonary disease · 2026Article
- Short-term cigarette smoke exposure aggravates oxidative stress and airway inflammation induced by lipopolysaccharides.Frontiers in physiology · 2026Article
- Less Is More: Silencing ANT1 Calms Lung Inflammation in Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2025Article
- ANT1 Deficiency Impairs Macrophage Metabolism and Migration, Protecting Against Emphysema in Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2025Article
- Single-Cell RNA Sequencing Identifies a Unique Macrophage Population in a Mouse Model of Ozone-induced Asthma Exacerbation.American journal of respiratory cell and molecular biology · 2025Article
- Naturally derived bioactive compounds as regulators of oxidative stress and inflammation in asthma.Chinese medicine · 2025Review
- A next-generation system for smoke inhalation integrated with a breathing lung-on-chip to model human lung responses to cigarette exposure.Scientific reports · 2025Article
- SignallingERJ open research · 2025Article
- BPIFB4 rs4339026 A > G polymorphism impacts COPD susceptibility in the Kashi population, China.Scientific reports · 2025Article
- The Mediation of Circulating Inflammatory Proteins in the Causal Pathway from Immune Cells to COPD.International journal of chronic obstructive pulmonary disease · 2025Article
- Differences in glycolytic metabolism between tissue-resident alveolar macrophages and recruited lung macrophages.Frontiers in immunology · 2025Review
- Advances on the Role of Lung Macrophages in the Pathogenesis of Chronic Obstructive Pulmonary Disease in the Era of Single-Cell Genomics.International journal of medical sciences · 2025Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Smoking is a leading risk factor of chronic obstructive pulmonary disease (COPD), that is characterized by chronic lung inflammation, tissue remodeling and emphysema. Although inflammation is critical to COPD pathogenesis, the cellular and molecular basis underlying smoking-induced lung inflammation and pathology remains unclear. Using murine smoke models and single-cell RNA-sequencing, we show that smoking establishes a self-amplifying inflammatory loop characterized by an influx of molecularly heterogeneous neutrophil subsets and excessive recruitment of monocyte-derived alveolar macrophages (MoAM). In contrast to tissue-resident AM, MoAM are absent in homeostasis and characterized by a pro-inflammatory gene signature. Moreover, MoAM represent 46% of AM in emphysematous mice and express markers causally linked to emphysema. We also demonstrate the presence of pro-inflammatory and tissue remodeling associated MoAM orthologs in humans that are significantly increased in emphysematous COPD patients. Inhibition of the IRAK4 kinase depletes a rare inflammatory neutrophil subset, diminishes MoAM recruitment, and alleviates inflammation in the lung of cigarette smoke-exposed mice. This study extends our understanding of the molecular signaling circuits and cellular dynamics in smoking-induced lung inflammation and pathology, highlights the functional consequence of monocyte and neutrophil recruitment, identifies MoAM as key drivers of the inflammatory process, and supports their contribution to pathological tissue remodeling.
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