ArticleThe American journal of pathology2000
Neutrophil priming by cigarette smoke condensate and a tobacco anti-idiotypic antibody.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 48 citations in OpenAlex.
- In vivo versus in vitro airway surface liquid nicotine levels following cigarette smoke exposure.Journal of analytical toxicology · 2008Trial
- The role of extracellular vesicles in COPD and potential clinical value.Respiratory research · 2024Review
- Unravelling the mechanisms driving multimorbidity in COPD to develop holistic approaches to patient-centred care.European respiratory review : an official journal of the European Respiratory Society · 2021Review
- The Interplay Between Immune Response and Bacterial Infection in COPD: Focus Upon Non-typeableFrontiers in immunology · 2018Review
- Electronic cigarette exposure triggers neutrophil inflammatory responses.Respiratory research · 2016Article
- Responsiveness of blood and sputum inflammatory cells in Japanese COPD patients, non-COPD smoking controls, and non-COPD nonsmoking controls.International journal of chronic obstructive pulmonary disease · 2016Article
- [Pulmonary Langerhans cell histiocytosis].Der Pathologe · 2015Review
- A novel nonhuman primate model of cigarette smoke-induced airway disease.The American journal of pathology · 2015Article
- Acute Immune-Inflammatory Responses to a Single Bout of Aerobic Exercise in Smokers; The Effect of Smoking History and Status.Frontiers in immunology · 2015Article
- Increased activation of blood neutrophils after cigarette smoking in young individuals susceptible to COPD.Respiratory research · 2014Article
- Importance of smoking and the occurrence of acute poisoning due to waterproof spray.Acute medicine & surgery · 2014Review
- Interstitial lung diseases-can pathologists arrive at an etiology-based diagnosis? A critical update.Virchows Archiv : an international journal of pathology · 2013Review
- Neutrophilic inflammatory response and oxidative stress in premenopausal women chronically exposed to indoor air pollution from biomass burning.Inflammation · 2012Article
- Cigarette smoke induces β2-integrin-dependent neutrophil migration across human endothelium.Respiratory research · 2011Article
- Immunomodulatory strategies prevent the development of autoimmune emphysema.Respiratory research · 2010Article
- Cholinergic activation of hematopoietic stem cells: role in tobacco-related disease?Vascular medicine (London, England) · 2010Article
- Glucocorticoid insensitivity as a future target of therapy for chronic obstructive pulmonary disease.International journal of chronic obstructive pulmonary disease · 2010Review
- S100A8 and S100A9 inhibit neutrophil oxidative metabolism in-vitro: involvement of adenosine metabolites.Free radical research · 2010Article
- Molecular pathogenesis of emphysema.The Journal of clinical investigation · 2008Review
- Future therapeutic treatment of COPD: struggle between oxidants and cytokines.International journal of chronic obstructive pulmonary disease · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A polyphenol-rich reagent, referred to as CSC, was isolated from cigarette smoke condensate and shown to prime purified human neutrophils. A mouse monoclonal anti-idiotypic antibody directed against the polyphenol-reactive determinants on a rabbit polyclonal anti-tobacco glycoprotein antibody was generated and shown to also prime neutrophils. After priming by CSC or tobacco anti-idiotypic antibody, there was a 2.5-fold to threefold increase in CD11b/18 expression and doubling of the number of formyl-methionyl-leucyl-phenylalanine receptors on the cells. The primed cells showed a twofold increase, compared with unprimed cells, in production of superoxide and release of neutrophil elastase after stimulation with formyl-methionyl-leucyl-phenylalanine. Neutrophils in peripheral blood of cigarette smokers have been shown to be primed and more responsive to activating agents. The priming effects attributed to whole cigarette smoke have been demonstrated in these studies using purified neutrophils and CSC or tobacco anti-idiotypic antibody. These studies are a first step in testing the hypothesis that the inflammatory process contributing to progression of chronic obstructive pulmonary disease in ex-smokers may be driven, in part, by tobacco anti-idiotypic antibodies. This hypothesis is novel and carries with it the implication of a heretofore unrecognized autoimmune component in the disease process manifested through production of anti-idiotypic antibodies with tobacco-like activity.
Indexed as
Identifiers
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.