ArticlePloS one2014
Induction of murine macrophage M2 polarization by cigarette smoke extract via the JAK2/STAT3 pathway.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 98 citations in OpenAlex.
- Simvastatin up-regulates adenosine deaminase and suppresses osteopontin expression in COPD patients through an IL-13-dependent mechanism.Respiratory research · 2016Trial
- 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 Inflammatory Roles of n-3 and n-6 Polyunsaturated Fatty Acids in COPD: Clinical Implications and Underlying Mechanisms.Journal of inflammation research · 2026Review
- Identifying therapeutic targets for allergic asthma through atopic dermatitis-associated genetic mechanisms.The journal of allergy and clinical immunology. Global · 2025Article
- Effects of Smoking on Macrophage Polarization in Peri-Implantitis Lesions.Clinical oral implants research · 2025Article
- The TRPA1 cation channel is upregulated by cigarette smoke in mouse and human macrophages modulating lung inflammation.Scientific reports · 2025Article
- Nicotine promotes M2 macrophage polarization through α5-nAChR/SOX2/CSF-1 axis in lung adenocarcinoma.Cancer immunology, immunotherapy : CII · 2024Article
- Macrophage Polarization and Functions in Pathogenesis of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2024Review
- CircRNA LOC729852 promotes bladder cancer progression by regulating macrophage polarization and recruitment via the miR-769-5p/IL-10 axis.Journal of cellular and molecular medicine · 2024Article
- Photodynamic Therapy and Adaptive Immunity Induced by Reactive Oxygen Species: Recent Reports.Cancers · 2024Review
- Lung Inflammatory Phenotype in Mice Deficient in Fibulin-2 and ADAMTS-12.International journal of molecular sciences · 2024Article
- Cigarette smoke sustains immunosuppressive microenvironment inducing M2 macrophage polarization and viability in lung cancer settings.PloS one · 2024Article
- Manipulating the tumor immune microenvironment to improve cancer immunotherapy: IGF1R, a promising target.Frontiers in immunology · 2024Review
- The Streptococcus virulence protein PepO triggers anti-tumor immune responses by reprograming tumor-associated macrophages in a mouse triple negative breast cancer model.Cell & bioscience · 2023Article
- AMolecules (Basel, Switzerland) · 2023Article
- Review
- Cancer and Alzheimer's Inverse Correlation: an Immunogenetic Analysis.Molecular neurobiology · 2023Review
- Article
- Alveolar macrophages in lung cancer: opportunities challenges.Frontiers in immunology · 2023Review
- Impact of JAK/STAT inhibitors on human monocyte-derived-macrophages stimulated by cigarette smoke extract and lipopolysaccharide.Clinical and experimental pharmacology & physiology · 2022Article
4 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
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cigarette smoking is a major pathogenic factor in lung cancer. Macrophages play an important role in host defense and adaptive immunity. These cells display diverse phenotypes for performing different functions. M2 type macrophages usually exhibit immunosuppressive and tumor-promoting characteristics. Although macrophage polarization toward the M2 phenotype has been observed in the lungs of cigarette smokers, the molecular basis of the process remains unclear. In this study, we evaluated the possible mechanisms for the polarization of mouse macrophages that are induced by cigarette smoking (CS) or cigarette smoke extract (CSE). The results showed that exposure to CSE suppressed the production of reactive oxygen species (ROS) and nitric oxide (NO) and down-regulated the phagocytic ability of Ana-1 cells. The CD163 expressions on the surface of macrophages from different sources were significantly increased in in vivo and in vitro studies. The M1 macrophage cytokines TNF-α, IL-12p40 and enzyme iNOS decreased in the culture supernatant, and their mRNA levels decreased depending on the time and concentration of CSE. In contrast, the M2 phenotype macrophage cytokines IL-10, IL-6, TGF-β1 and TGF-β2 were up-regulated. Moreover, phosphorylation of JAK2 and STAT3 was observed after the Ana-1 cells were treated with CSE. In addition, pretreating the Ana-1 cells with the STAT3 phosphorylation inhibitor WP1066 inhibited the CSE-induced CD163 expression, increased the mRNA level of IL-10 and significantly decreased the mRNA level of IL-12. In conclusion, we demonstrated that the M2 polarization of macrophages induced by CS could be mediated through JAK2/STAT3 pathway activation.
Indexed as
Identifiers
What OpenQuestion holds
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.