ArticleScientific reports2020
Alteration of immunophenotype of human macrophages and monocytes after exposure to cigarette smoke.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- Cigarette smoke destabilizes G-quadruplex structures and antagonizes G4-ligand effects in macrophages.Scientific reports · 2025Article
- A translational view of airway epithelial dysfunction in COPD.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Senkyunolide H reverses depression-induced breast cancer progression by regulating CXCR2.Natural products and bioprospecting · 2025Article
- Differences in the Inflammatory Response and Corticoid Responsiveness of Human Lung Macrophages and Parenchymal Explants Exposed to Cigarette Smoke Extracts.Basic & clinical pharmacology & toxicology · 2025Article
- Dysregulated NK cell activation and myeloid-lymphoid imbalance underpin COPD progression: insights from high-dimensional immune profiling and smoking-induced immune remodeling.Frontiers in immunology · 2025Article
- Targeting CCL2-CCR2 signaling pathway alleviates macrophage dysfunction in COPD via PI3K-AKT axis.Cell communication and signaling : CCS · 2024Article
- Dual Exposure to E-Cigarette Vapour and Cigarette Smoke Results in Poorer Airway Cell, Monocyte, and Macrophage Function Than Single Exposure.International journal of molecular sciences · 2024Article
- Inhalation of nicotine-containing electronic cigarette vapor exacerbates the features of COPD by inducing ferroptosis in βENaC-overexpressing mice.Frontiers in immunology · 2024Article
- Caspase-8 activation by cigarette smoke induces pro-inflammatory cell death of human macrophages exposed to lipopolysaccharide.Cell death & disease · 2023Article
- Live to die another day: novel insights may explain the pathophysiology behind smoker's paradox in SARS-CoV-2 infection.Molecular and cellular biochemistry · 2023Review
- COPD Patients Exhibit Distinct Gene Expression, Accelerated Cellular Aging, and Bias to M2 Macrophages.International journal of molecular sciences · 2023Article
- A Pilot Cross-Sectional Study of Immunological and Microbiome Profiling Reveals Distinct Inflammatory Profiles for Smokers, Electronic Cigarette Users, and Never-Smokers.Microorganisms · 2023Article
- Immunoprofiling bronchoalveolar lavage cells reveals multifaceted smoking-associated immune dysfunction.ERJ open research · 2023Article
- Matrix Metalloproteinases in Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2023Review
- The Potential Importance of CXCL1 in the Physiological State and in Noncancer Diseases of the Cardiovascular System, Respiratory System and Skin.International journal of molecular sciences · 2022Review
- Impact of JAK/STAT inhibitors on human monocyte-derived-macrophages stimulated by cigarette smoke extract and lipopolysaccharide.Clinical and experimental pharmacology & physiology · 2022Article
- Cigarette smoke exposed airway epithelial cell-derived EVs promote pro-inflammatory macrophage activation in alpha-1 antitrypsin deficiency.Respiratory research · 2022Article
- Article
- Cigarette smoke promotes oral leukoplakia via regulating glutamine metabolism and M2 polarization of macrophage.International journal of oral science · 2021Article
- Development and validation of a mouse model of contemporary cannabis smoke exposure.ERJ open research · 2021Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cigarette smoke exposure (CS) is the main risk factor for chronic obstructive pulmonary disease (COPD). Macrophages have an important role in COPD because they release pro-inflammatory and anti-inflammatory cytokines. The present study's we investigate the functional changes in macrophages and monocytes exposed to cigarette smoke extract (CSE). Herein, using human monocyte-derived macrophages (MDMs) from healthy donors and we found that CSE was not associated with significant changes in the production of pro inflammatory cytokines by MDMs. In contrast, exposure to CSE suppressed the production of IL-6 and Gro-a/CXCL1 by LPS-stimulated-MDMs, but had an additive effect on the release of IL-8/CXCL8 and MCP1/CCL2. However, CSE exposure was associated with greater production, TARC/CCL-17 and CCL22/MDC. Moreover, MDMs displayed a lower uptake capacity after CSE exposure. We identify, for what is to our knowledge the first time that monocytes from patients with COPD produced less IL-8/CXCL8 and Gro-α/CXCL1 after LPS stimulation and produced higher levels of TARC/CCL17 and MDC/CCL-22 after IL-4 stimulation. Our present results highlighted a skewed immune response, with an imbalance in M1 vs. M2 cytokine production. In conclusion, exposure to CS has contrasting, multifaceted effects on macrophages and monocytes. Our data may provide a better understanding of the mechanisms underlying COPD.
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Registered trials
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