ArticleRespiratory research2017
Cigarette smoke destabilizes NLRP3 protein by promoting its ubiquitination.
Article in Respiratory research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
- Cigarette and Electronic Cigarette Exposure in Osteoarthritis: Immune Dysregulation and Inflammatory Signaling Pathways.International journal of general medicine · 2026Article
- Serum DIP2C protein concentration in human colorectal cancer among Yemeni patients.Frontiers in oncology · 2026Article
- The Role of Ubiquitination and Deubiquitination in the Pathogenesis of Acute Kidney Injury: Progress in Research.Biomedicines · 2025Review
- Attenuation of NLRP3 Inflammasome by Cigarette Smoke is Correlated with Decreased Defense Response of Oral Epithelial Cells toCurrent molecular medicine · 2024Article
- Comparison of Pollutant Effects on Cutaneous Inflammasomes Activation.International journal of molecular sciences · 2023Article
- Pulmonary immune response regulation, genotoxicity, and metabolic reprogramming by menthol- and tobacco-flavored e-cigarette exposures in mice.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- Reframing the link between metabolism and NLRP3 inflammasome: therapeutic opportunities.Frontiers in immunology · 2023Review
- Polyphenols, flavonoids and inflammasomes: the role of cigarette smoke in COPD.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Inflammasome involvement in CS-induced damage in HaCaT keratinocytes.In vitro cellular & developmental biology. Animal · 2022Article
- USP13 Deficiency Aggravates Cigarette-smoke-induced Alveolar Space Enlargement.Cell biochemistry and biophysics · 2021Article
- Roles of Inflammasome in Cigarette Smoke-Related Diseases and Physiopathological Disorders: Mechanisms and Therapeutic Opportunities.Frontiers in immunology · 2021Review
- NLRP3 Inflammasome is Activated in Rat Pancreatic Islets by Transplantation and Hypoxia.Scientific reports · 2020Article
- Cigarette smoke extract modulatesAmerican journal of physiology. Lung cellular and molecular physiology · 2020Article
- E-cigarettes: Effects in phagocytosis and cytokines response against Mycobacterium tuberculosis.PloS one · 2020Article
- Control of the inflammasome by the ubiquitin system.The FEBS journal · 2020Review
- The role of cigarette smoke-induced epigenetic alterations in inflammation.Epigenetics & chromatin · 2019Review
- Exploring the Involvement of NLRP3 and IL-1Mediators of inflammation · 2019Article
- The inflammasomes, immune guardians at defence barriers.Immunology · 2018Review
- Tobacco Smoke Induces and Alters Immune Responses in the Lung Triggering Inflammation, Allergy, Asthma and Other Lung Diseases: A Mechanistic Review.International journal of environmental research and public health · 2018Review
- Spotlight on the NLRP3 inflammasome pathway.Journal of inflammation research · 2018Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCigarette smoke suppresses innate immunity, making smokers more susceptible to infection. The NLRP3 inflammasome is a multi-protein complex that releases interleukin (IL) -1β and IL -18. These cytokines are critical for a timely host response to pathogens. Whether cigarette smoke affects NLRP3 protein levels, and its ability to form an inflammasome, is not known. METHODS AND
resultsUsing the human monocyte THP1 cell line and C57BL/6 mice, we show that cigarette smoke decreases NLRP3 levels in cells by increasing ubiquitin-mediated proteasomal processing. Half-life of NLRP3 is shortened with the exposure to cigarette smoke extract. Cigarette smoke extract reduces cellular NLRP3 protein abundance in the presence of lipopolysaccharide, a known inducer of NLRP3 protein, thereby decreasing the formation of NLRP3 inflammasomes. The release of IL-1β and IL-18 by inflammasome activation is also decreased with the exposure to cigarette smoke extract both in THP1 cells and primary human peripheral blood macrophages.
conclusionsCigarette smoke extract decreased NLRP3 protein abundance via increased ubiquitin-mediated proteasomal processing. The release of IL-1β and IL-18 is also decreased with cigarette smoke extract. Our findings may provide mechanistic insights on immunosuppression in smokers and unique opportunities to develop a strategy to modulate immune function.
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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.