ArticlePloS one2014
IL-17A and serum amyloid A are elevated in a cigarette smoke cessation model associated with the persistence of pigmented macrophages, neutrophils and activated NK cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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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.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- Cytotoxic lymphocytes in COPD airways: increased NK cells associated with disease, iNKT and NKT-like cells with current smoking.Respiratory research · 2018Trial
- Role of Th17 cells, Treg cells, and Th17/Treg imbalance in immune homeostasis disorders in patients with chronic obstructive pulmonary disease.Immunity, inflammation and disease · 2023Review
- Serum Amyloid A in Stable Patients with Chronic Obstructive Pulmonary Disease Does Not Reflect the Clinical Course of the Disease.International journal of molecular sciences · 2023Article
- Cigarette smoke stimulates clonal expansion of Jak2Frontiers in oncology · 2023Article
- Article
- Enhanced lung inflammatory response in whole-body compared to nose-only cigarette smoke-exposed mice.Respiratory research · 2021Article
- Emerging Biological Functions of IL-17A: A New Target in Chronic Obstructive Pulmonary Disease?Frontiers in pharmacology · 2021Review
- Electronic-Cigarette Vehicles and Flavoring Affect Lung Function and Immune Responses in a Murine Model.International journal of molecular sciences · 2020Article
- Long-Term Sequelae of Smoking and Cessation in Spontaneously Hypertensive Rats.Toxicologic pathology · 2020Article
- Sex differences in lymphoid follicles in COPD airways.Respiratory research · 2020Article
- Senescence in Pulmonary Fibrosis: Between Aging and Exposure.Frontiers in medicine · 2020Review
- Changes in the expression level of IL-17A and p53-fibrinolytic system in smokers with or without COPD.Molecular biology reports · 2018Article
- Granulocyte-CSF links destructive inflammation and comorbidities in obstructive lung disease.The Journal of clinical investigation · 2018Article
- COPD and squamous cell lung cancer: aberrant inflammation and immunity is the common link.British journal of pharmacology · 2016Review
- Structure and Expression of Different Serum Amyloid A (SAA) Variants and their Concentration-Dependent Functions During Host Insults.Current medicinal chemistry · 2016Review
- Innate cellular sources of interleukin-17A regulate macrophage accumulation in cigarette- smoke-induced lung inflammation in mice.Clinical science (London, England : 1979) · 2015Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While global success in cessation advocacy has seen smoking rates fall in many developed countries, persistent lung inflammation in ex-smokers is an increasingly important clinical problem whose mechanistic basis remains poorly understood. In this study, candidate effector mechanisms were assessed in mice exposed to cigarette smoke (CS) for 4 months following cessation from long term CS exposure. BALF neutrophils, CD4+ and CD8+ T cells and lung innate NK cells remained significantly elevated following smoking cessation. Analysis of neutrophil mobilization markers showed a transition from acute mediators (MIP-2α, KC and G-CSF) to sustained drivers of neutrophil and macrophage recruitment and activation (IL-17A and Serum Amyoid A (SAA)). Follicle-like lymphoid aggregates formed with CS exposure and persisted with cessation, where they were in close anatomical proximity to pigmented macrophages, whose number actually increased 3-fold following CS cessation. This was associated with the elastolytic protease, MMP-12 (macrophage metallo-elastase) which remained significantly elevated post-cessation. Both GM-CSF and CSF-1 were significantly increased in the CS cessation group relative to the control group. In conclusion, we show that smoking cessation mediates a transition to accumulation of pigmented macrophages, which may contribute to the expanded macrophage population observed in COPD. These macrophages together with IL-17A, SAA and innate NK cells are identified here as candidate persistence determinants and, we suggest, may represent specific targets for therapies directed towards the amelioration of chronic airway inflammation.
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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.