ArticlePloS one2015
Increased Protease-Activated Receptor-2 (PAR-2) Expression on CD14++CD16+ Peripheral Blood Monocytes of Patients with Severe Asthma.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Review
- Vascular remodeling and TSLP/angiogenin overexpression in severe mixed asthma.Respiratory research · 2025Article
- Sex differences in asthma control, lung function and exacerbations: the ATLANTIS study.BMJ open respiratory research · 2024Observational
- Association of single nucleotide polymorphisms in the F2RL1 gene with clinical and inflammatory characteristics of patients with asthma.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2024Article
- Review
- β-Arrestin-biased proteinase-activated receptor-2 antagonist C781 limits allergen-induced airway hyperresponsiveness and inflammation.British journal of pharmacology · 2023Article
- Protease-activated receptors in health and disease.Physiological reviews · 2023Review
- Proteinase-activated receptor-2 antagonist C391 inhibits Alternaria-induced airway epithelial signalling and asthma indicators in acute exposure mouse models.British journal of pharmacology · 2022Article
- Protease-activated receptor-2: Role in asthma pathogenesis and utility as a biomarker of disease severity.Frontiers in medicine · 2022Review
- Involvement of Neuro-Immune Interactions in Pruritus With Special Focus on Receptor Expressions.Frontiers in medicine · 2021Review
- Review
- Stability of peripheral blood immune markers in patients with asthma.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2019Article
- Protease-activated receptor-2 signaling through β-arrestin-2 mediates Alternaria alkaline serine protease-induced airway inflammation.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Dendritic Cell Subsets in Asthma: Impaired Tolerance or Exaggerated Inflammation?Frontiers in immunology · 2017Review
- Protective Roles for RGS2 in a Mouse Model of House Dust Mite-Induced Airway Inflammation.PloS one · 2017Article
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Authors and funding
9 authors.
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Abstract
backgroundProtease-Activated Receptor-2 (PAR-2), a G protein coupled receptor activated by serine proteases, is widely expressed in humans and is involved in inflammation. PAR-2 activation in the airways plays an important role in the development of allergic airway inflammation. PAR-2 expression is known to be upregulated in the epithelium of asthmatic subjects, but its expression on immune and inflammatory cells in patients with asthma has not been studied.
methodsWe recruited 12 severe and 24 mild/moderate asthmatics from the University of Alberta Hospital Asthma Clinics and collected baseline demographic information, medication use and parameters of asthma severity. PAR-2 expression on blood inflammatory cells was analyzed by flow cytometry.
resultsSubjects with severe asthma had higher PAR-2 expression on CD14++CD16+ monocytes (intermediate monocytes) and also higher percentage of CD14++CD16+PAR-2+ monocytes (intermediate monocytes expressing PAR-2) in blood compared to subjects with mild/moderate asthma. Receiver operating characteristics (ROC) curve analysis showed that the percent of CD14++CD16+PAR-2+ in peripheral blood was able to discriminate between patients with severe and those with mild/moderate asthma with high sensitivity and specificity. In addition, among the whole populations, subjects with a history of asthma exacerbations over the last year had higher percent of CD14++CD16+ PAR-2+ cells in peripheral blood compared to subjects without exacerbations.
conclusionsPAR-2 expression is increased on CD14++CD16+ monocytes in the peripheral blood of subjects with severe asthma and may be a biomarker of asthma severity. Our data suggest that PAR-2 -mediated activation of CD14++CD16+ monocytes may play a role in the pathogenesis of severe asthma.
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