ArticleAmerican journal of respiratory cell and molecular biology2017
Nicotine Impairs Macrophage Control of Mycobacterium tuberculosis.
Article in American journal of respiratory cell and molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 53 citations in OpenAlex.
- The triple-hit hypothesis: exploring pulmonary e-cigarette, PMEuropean respiratory review : an official journal of the European Respiratory Society · 2026Review
- Associations of exposure to ambient PMBMC public health · 2026Article
- Effect of Nicotine on Pulmonary Pathogenic Bacteria.Current microbiology · 2024Review
- Nicotinic regulation of microglia: potential contributions to addiction.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Cigarette Smoking as a Risk Factor for Tuberculosis in Adults: Epidemiology and Aspects of Disease Pathogenesis.Pathogens (Basel, Switzerland) · 2024Review
- The Role of the Acetylcholine System in Common Respiratory Diseases and COVID-19.Molecules (Basel, Switzerland) · 2023Review
- Article
- Effect of Nicotine on Immune System Function.Advanced pharmaceutical bulletin · 2023Review
- Nicotine Suppresses Phagocytic Ability of Macrophages by Regulating the miR-296-3p-SIRPAnalytical cellular pathology (Amsterdam) · 2023Article
- α1-Antitrypsin Binds to the Glucocorticoid Receptor with Anti-Inflammatory and Antimycobacterial Significance in Macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Diagnostic Efficacy of T-SPOT.TB for Active Tuberculosis in Adult: A Retrospective Study.Infection and drug resistance · 2022Article
- Review
- Cholinergic System and Its Therapeutic Importance in Inflammation and Autoimmunity.Frontiers in immunology · 2021Review
- Divergent Effect of Cigarette Smoke on Innate Immunity in Inflammatory Bowel Disease: A Nicotine-Infection Interaction.International journal of molecular sciences · 2020Review
- Mystery Solved: Why Smoke Extract Worsens Disease in Smokers with Crohn's Disease and Not Ulcerative Colitis? Gut MAP!Microorganisms · 2020Article
- Nicotine modulates molecules of the innate immune response in epithelial cells and macrophages during infection with M. tuberculosis.Clinical and experimental immunology · 2020Article
- E-cigarettes: Effects in phagocytosis and cytokines response against Mycobacterium tuberculosis.PloS one · 2020Article
- The Cholinergic System Contributes to the Immunopathological Progression of Experimental Pulmonary Tuberculosis.Frontiers in immunology · 2020Article
- Cigarette smoke-induced HMGB1 translocation and release contribute to migration and NF-κB activation through inducing autophagy in lung macrophages.Journal of cellular and molecular medicine · 2020Article
- Nicotine Impairs the Response of Lung Epithelial Cells to IL-22.Mediators of inflammation · 2020Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Pure nicotine impairs macrophage killing of Mycobacterium tuberculosis (MTB), but it is not known whether the nicotine component in cigarette smoke (CS) plays a role. Moreover, the mechanisms by which nicotine impairs macrophage immunity against MTB have not been explored. To neutralize the effects of nicotine in CS extract, we used a competitive inhibitor to the nicotinic acetylcholine receptor (nAChR)-mecamylamine-as well as macrophages derived from mice with genetic disruption of specific subunits of nAChR. We also determined whether nicotine impaired macrophage autophagy and whether nicotine-exposed T regulatory cells (Tregs) could subvert macrophage anti-MTB immunity. Mecamylamine reduced the CS extract increase in MTB burden by 43%. CS extract increase in MTB was also significantly attenuated in macrophages from mice with genetic disruption of either the α7, β2, or β4 subunit of nAChR. Nicotine inhibited autophagosome formation in MTB-infected THP-1 cells and primary murine alveolar macrophages, as well as increased the intracellular MTB burden. Nicotine increased migration of THP-1 cells, consistent with the increased number of macrophages found in the lungs of smokers. Nicotine induced Tregs to produce transforming growth factor-β. Naive mouse macrophages co-cultured with nicotine-exposed Tregs had significantly greater numbers of viable MTB recovered with increased IL-10 production and urea production, but no difference in secreted nitric oxide as compared with macrophages cocultured with unexposed Tregs. We conclude that nicotine in CS plays an important role in subverting macrophage control of MTB infection.
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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.