ArticleIn vitro cellular & developmental biology. Animal2020
Effect of CSE on M1/M2 polarization in alveolar and peritoneal macrophages at different concentrations and exposure in vitro.
Article in In vitro cellular & developmental biology. Animal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.
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Who cites it
17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 32 citations in OpenAlex.
- The interplay between oxidative stress and autophagy in chronic obstructive pulmonary disease.Frontiers in physiology · 2022Pooled it
- The molecular mechanism of ferroptosis and its role in COPD.Frontiers in medicine · 2022Pooled it
- 4-(5'-Dimethylamino)-Naphthalenesulfonyl-2(3H)-Benzoxazolone (W3D) Ameliorated COPD Lung Injury Through Regulating Macrophage Polarization Mediated by Glycolysis.Archiv der Pharmazie · 2026Article
- Vaping induces a marked pro-inflammatory state within the lung, which is at least partially due to its immunomodulatory effects.Frontiers in immunology · 2026Article
- The global burden of chronic respiratory diseases attributable to tobacco from 1990 to 2021: a global burden of disease study 2021.BMC public health · 2025Article
- PGAM5 Modulates Macrophage Polarization, Aggravating Inflammation in COPD via the NF-κB Pathway.International journal of chronic obstructive pulmonary disease · 2025Article
- Bexarotene ameliorated the pulmonary inflammation and M1 polarization of alveolar macrophages induced by cigarette smoke via PPARγ/HO-1.Respiratory research · 2024Article
- SARS-CoV-2 Modulation of HIV Latency Reversal in a Myeloid Cell Line: Direct and Bystander Effects.Viruses · 2024Article
- Melatonin improves influenza virus infection-induced acute exacerbation of COPD by suppressing macrophage M1 polarization and apoptosis.Respiratory research · 2024Article
- Article
- Copper homeostasis dysregulation in respiratory diseases: a review of current knowledge.Frontiers in physiology · 2024Review
- Cigarette smoke sustains immunosuppressive microenvironment inducing M2 macrophage polarization and viability in lung cancer settings.PloS one · 2024Article
- Cigarette smoke increases susceptibility of alveolar macrophages to SARS-CoV-2 infection through inducing reactive oxygen species-upregulated angiotensin-converting enzyme 2 expression.Scientific reports · 2023Article
- Characterization of a novel galectin inFrontiers in microbiology · 2023Article
- The roles of long noncoding RNA-mediated macrophage polarization in respiratory diseases.Frontiers in immunology · 2022Review
- NCOA4-Mediated Ferroptosis in Bronchial Epithelial Cells Promotes Macrophage M2 Polarization in COPD Emphysema.International journal of chronic obstructive pulmonary disease · 2022Article
- The inhibitor miR-21 regulates macrophage polarization in an experimental model of chronic obstructive pulmonary disease.Tobacco induced diseases · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Cigarette smoke exposure is one of the main etiologies for chronic obstructive pulmonary disease. Moreover, cigarette smoke participates in disease progression by inducing abnormal macrophage polarization; however, the effects of cigarette smoke on M1/M2 macrophage polarization have not been established. The aim of the current study was to determine the effects of cigarette smoke extract (CSE) on M1/M2 macrophage polarization in alveolar and peritoneal macrophages (AM and PM, respectively) at different concentrations and exposure times. Rat AM and PM were cultured with CSE at different concentrations. CCK-8 was used as an indicator of cell viability, and mRNA expression of M1 (iNOS, TNF-α, and IL-1β) and M2 markers (arg-1, CD206, and TGF-β1) were measured at 3, 6, 9, 12, and 24 h using qPCR. Expressions of CD86 and CD206 proteins at 12 h were determined using flow cytometry, and the iNOS/arg-1 ratio was used to determine the polarization dominance of M1 and M2. M2 subtypes were detected at 12 h using qPCR and flow cytometry. CSE increased the expression of iNOS, TNF-α, and IL-1β mRNA, and the proportion of CD86-positive cells in AM and PM promoted M1 polarization, and M1 polarization was continuously enhanced as exposure time and concentration increased. CSE reduced the expression of arg-1, CD206, and TGF-β1 mRNA and the proportion of CD206-positive cells in AM and PM and inhibited M2 polarization. At 9-24 h of CSE exposure, the expression of arg-1 in AM and PM gradually increased, showing tendency towards activation of M2 polarization. Besides, CSE might induce M2b and M2d polarization at 12 h. After 12 h of CSE exposure, transformation from M1 to M2 polarization dominance was shown in AM; however, M1 polarization was continuously enhanced in PM within 24 h of CSE exposure. CSE promoted M1 polarization in macrophages, exhibiting dynamic regulatory effects on M2 polarization, first as a suppressor and then as a promoter. The polarization change induced by CSE on AM was more sensitive than PM.
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