ArticleClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology2018
Neutrophilia, gelatinase release and microvascular leakage induced by human mast cell tryptase in a mouse model: Lack of a role of protease-activated receptor 2 (PAR2).
Article in Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Synovial mast cells and osteoarthritis: Current understandings and future perspectives.Heliyon · 2024Review
- Pruritogens in pemphigoid diseases: Possible therapeutic targets for a burdensome symptom.The Journal of dermatology · 2023Review
- Biomarkers and Their Possible Functions in the Intestinal Microenvironment of Chagasic Megacolon: An Overview of the (Neuro)inflammatory Process.Journal of immunology research · 2021Review
- Expression of Inflammatory Markers RANK, MMP-9 and PTHrP in Chronic Apical Periodontitis from People Living with HIV Undergoing Antiretroviral Therapy.Journal of clinical medicine · 2020Article
- Effect of tryptase on mouse brain microvascular endothelial cells via protease-activated receptor 2.Journal of neuroinflammation · 2018Article
- Neutrophilia, gelatinase release and microvascular leakage induced by human mast cell tryptase in a mouse model: Lack of a role of protease-activated receptor 2 (PAR2).Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2018Article
- Glia Maturation Factor and Mast Cell-Dependent Expression of Inflammatory Mediators and Proteinase Activated Receptor-2 in Neuroinflammation.Journal of Alzheimer's disease : JAD · 2018Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundTryptase, the most abundant protease of the human mast cell, has been implicated as a key mediator of allergic inflammation that acts through activation of PAR2.
objectivesTo investigate the contribution of PAR2 in the pro-inflammatory actions mediated by tryptase in a mice model.
methodsWe have injected recombinant human βII-tryptase into the peritoneum of PAR2-deficient and wild-type C57BL/6 mice. After 6, 12 and 24 hours, mice were killed, peritoneal lavage performed and inflammatory changes investigated.
resultsTryptase stimulated an increase in neutrophil numbers in the peritoneum, but responses did not differ between PAR2-deficient and wild-type mice. Heat inactivation of tryptase or pre-incubation with a selective tryptase inhibitor reduced neutrophilia, but neutrophil accumulation was not elicited with a peptide agonist of PAR2 (SLIGRL-NH
conclusionsOur findings indicate that tryptase is a potent stimulus for neutrophil accumulation, MMP release and microvascular leakage. Although these actions required an intact catalytic site, the primary mechanism of tryptase in vivo would appear to involve processes independent of PAR2.
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Registered trials
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