ArticlePhysiological reports2015
Cigarette smoke represses the innate immune response to asbestos.
Article in Physiological reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Methylation-derived Neutrophil-to-Lymphocyte Ratio and Lung Cancer Risk in Heavy Smokers.Cancer prevention research (Philadelphia, Pa.) · 2018Trial
- The Convergent Immunopathogenesis of Cigarette Smoke Exposure: From Oxidative Stress to Epigenetic Reprogramming in Chronic Disease.International journal of molecular sciences · 2025Review
- Attenuation of NLRP3 Inflammasome by Cigarette Smoke is Correlated with Decreased Defense Response of Oral Epithelial Cells toCurrent molecular medicine · 2024Article
- Polyphenols, flavonoids and inflammasomes: the role of cigarette smoke in COPD.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Role of the Synergistic Interactions of Environmental Pollutants in the Development of Cancer.GeoHealth · 2022Review
- The Acute Toxicity of Mineral Fibres: A Systematic In Vitro Study Using Different THP-1 Macrophage Phenotypes.International journal of molecular sciences · 2022Article
- Cigarette smoke-induced gasdermin D activation in bronchoalveolar macrophages and bronchial epithelial cells dependently on NLRP3.Frontiers in immunology · 2022Article
- Asbestos, Smoking and Lung Cancer: An Update.International journal of environmental research and public health · 2019Review
- The inflammasomes, immune guardians at defence barriers.Immunology · 2018Review
- An observation on the severity of periodontal disease in past cigarette smokers suffering from rheumatoid arthritis- evidence for a long-term effect of cigarette smoke exposure?BMC oral health · 2018Article
- Cigarette smoke destabilizes NLRP3 protein by promoting its ubiquitination.Respiratory research · 2017Article
- Cigarette smoke represses the innate immune response to asbestos.Physiological reports · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Both cigarette smoke (CS) and asbestos cause lung inflammation and lung cancer, and at high asbestos exposure levels, populations exposed to both of these carcinogens display a synergistic increase in the development of lung cancer. The mechanisms through which these two toxic agents interact to promote lung tumorigenesis are poorly understood. Here, we begin to dissect the inflammatory signals induced by asbestos in combination with CS using a rodent inhalation model and in vitro cell culture. Wild-type C57BL/6 mice were exposed to room air as a control, CS, and/or asbestos (4 days per week to CS and 1 day per week to asbestos for 5 weeks). Bronchoalveolar lavage (BAL) fluid was collected following exposure and analyzed for inflammatory mediators. Asbestos-exposed mice displayed an increased innate immune response consistent with NLRP3 inflammasome activation. Compared to mice exposed only to asbestos, animals coexposed to CS + asbestos displayed attenuated levels of innate immune mediators and altered inflammatory cell recruitment. Histopathological changes in CS + asbestos-exposed mice correlated with attenuated fibroproliferative lesion development relative to their counterparts exposed only to asbestos. In vitro experiments using a human monocyte cell line (THP-1 cells) supported the in vivo results in that coexposure to cigarette smoke extract repressed NLRP3 inflammasome markers in cells treated with asbestos. These observations indicate that CS represses central components of the innate immune response to inhaled asbestos.
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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.