ArticleInternational journal of chronic obstructive pulmonary disease2016
Interleukin-16-producing NK cells and T-cells in the blood of tobacco smokers with and without COPD.
Article in International journal of chronic obstructive pulmonary disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Genetic and Molecular Interconnections Between Chronic Obstructive Pulmonary Disease and Osteoporosis: Insights from Single-Cell and Mendelian Randomization Analyses.International journal of chronic obstructive pulmonary disease · 2026Article
- Dynamic changes of immune cells and therapeutic responses in experimental models of COPD.Frontiers in immunology · 2026Review
- Role of interleukin-16 in human diseases: a novel potential therapeutic target.Frontiers in immunology · 2025Review
- Natural Killer Cells as a Further Insight into the Course of Chronic Obstructive Pulmonary Disease.Biomedicines · 2024Article
- Article
- Interleukin (IL) 16: a candidate urinary biomarker for proliferative lupus nephritis.Lupus science & medicine · 2022Article
- Biomarkers, Clinical Course, and Individual Needs in COPD Patients in Primary Care: The Study Protocol of the Stockholm COPD Inflammation Cohort (SCOPIC).International journal of chronic obstructive pulmonary disease · 2022Article
- 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
- Association of mean platelet volume with incident type 2 diabetes mellitus risk: the Dongfeng-Tongji cohort study.Diabetology & metabolic syndrome · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLong-term exposure to tobacco smoke causes local inflammation in the airways that involves not only innate immune cells, including NK cells, but also adaptive immune cells such as cytotoxic (CD8
methodsWe quantified extracellular IL-16 protein (ELISA) and intracellular IL-16 in NK cells, T-cells, B-cells, and monocytes (flow cytometry) in blood samples from long-term tobacco smokers with and without chronic obstructive pulmonary disease (COPD) and in never-smokers. NK cells from healthy blood donors were stimulated with water-soluble tobacco smoke components (cigarette smoke extract) with or without an OFR scavenger (glutathione) in vitro and followed by quantification of IL-16 protein.
resultsThe extracellular concentrations of IL-16 protein in blood did not display any substantial differences between groups. Notably, intracellular IL-16 protein was detected in all types of blood leukocytes. All long-term smokers displayed a decrease in this IL-16 among NK cells, irrespective of COPD status. Further, both NK and CD4
conclusionLong-term exposure to tobacco smoke does not markedly alter extracellular concentrations of IL-16 protein in blood. However, it does decrease the intracellular IL-16 concentrations in blood NK cells, the latter effect involving OFR. Thus, long-term tobacco smoking exerts an impact at the systemic level that involves NK cells; innate immune cells that are critical for host defense against viruses and tumors - conditions that are overrepresented among smokers.
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