ArticleCell death & disease2011
Cigarette smoke-exposed neutrophils die unconventionally but are rapidly phagocytosed by macrophages.
Article in Cell death & disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 55 citations in OpenAlex.
- The implication of cigarette smoking and cessation on macrophage cholesterol efflux in coronary artery disease patients.Journal of lipid research · 2015Trial
- Pathogenic Cell in COPD: Mechanisms of Airway Remodeling, Immune Dysregulation, and Therapeutic Implications.International journal of chronic obstructive pulmonary disease · 2025Review
- Cigarette Smoke-Induced Respiratory Response: Insights into Cellular Processes and Biomarkers.Antioxidants (Basel, Switzerland) · 2023Review
- A Macrophage-Related Gene Signature for Identifying COPD Based on Bioinformatics and ex vivo Experiments.Journal of inflammation research · 2023Article
- Tobacco smoke exacerbates Filifactor alocis pathogenicity.Journal of clinical periodontology · 2023Article
- Review
- Liproxstatin‑1 induces cell cycle arrest, apoptosis, and caspase‑3/GSDME‑dependent secondary pyroptosis in K562 cells.International journal of oncology · 2022Article
- No smoke without fire: the impact of cigarette smoking on the immune control of tuberculosis.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Blocking the human common beta subunit of the GM-CSF, IL-5 and IL-3 receptors markedly reduces hyperinflammation in ARDS models.Cell death & disease · 2022Article
- Neutrophils in chronic inflammatory diseases.Cellular & molecular immunology · 2022Review
- E-cigarettes and health risks: more to the flavor than just the name.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Orchestration of Neutrophil Extracellular Traps (Nets), a Unique Innate Immune Function during Chronic Obstructive Pulmonary Disease (COPD) Development.Biomedicines · 2021Review
- Neutrophils Modulate Fibrogenesis in Chronic Pulmonary Diseases.Frontiers in medicine · 2021Review
- Coronavirus Disease 2019 and Smoking: How and Why We Implemented a Tobacco Treatment Campaign.Chest · 2020Review
- Autophagy in chronic lung disease.Progress in molecular biology and translational science · 2020Review
- Exposure to Cigarette Smoke Augments Post-ischemic Brain Injury and Inflammation via Mobilization of Neutrophils and Monocytes.Frontiers in immunology · 2019Article
- Acute pulmonary effects of aerosolized nicotine.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Tobacco-induced suppression of the vascular response to dental plaque.Molecular oral microbiology · 2018Review
- Toll-like receptor 2 activation primes and upregulates osteoclastogenesis via lox-1.Lipids in health and disease · 2018Article
- Cessation from Smoking Improves Innate Host Defense and Clearance of Experimentally Inoculated Nasal Staphylococcus aureus.Infection and immunity · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Pulmonary accumulation of neutrophils is typical for active smokers who are also predisposed to multiple inflammatory and infectious lung diseases. We show that human neutrophil exposure to cigarette smoke extract (CSE) leads to an atypical cell death sharing features of apoptosis, autophagy and necrosis. Accumulation of tar-like substances in autophagosomes is also apparent. Before detection of established cell death markers, CSE-treated neutrophils are effectively recognized and non-phlogistically phagocytosed by monocyte-derived macrophages. Blockade of LOX-1 and scavenger receptor A, but not MARCO or CD36, as well as pre-incubation with oxLDL, inhibited phagocytosis, suggesting that oxLDL-like structures are major phagocytosis signals. Specific lipid (β-carotene and quercetin), but not aqueous, antioxidants increased the pro-phagocytic effects of CSE. In contrast to non-phlogistic phagocytosis, degranulation of secondary granules, as monitored by lactoferrin release, was apparent on CSE exposure, which is likely to promote pulmonary inflammation and tissue degradation. Furthermore, CSE-exposed neutrophils exhibited a compromised ability to ingest the respiratory pathogen, Staphylococcus aureus, which likely contributes to bacterial persistence in the lungs of smokers and is likely to promote further pulmonary recruitment of neutrophils. These data provide mechanistic insight into the lack of accumulation of apoptotic neutrophil populations in the lungs of smokers and their increased susceptibility to degradative pulmonary diseases and bacterial infections.
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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.