ArticleClinical and molecular allergy : CMA2021
The blocking effect of the glycoprotein IIb/IIIa receptor in the mouse model of asthma.
Article in Clinical and molecular allergy : CMA, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Blood Transfusion Components Inducing Severe Allergic Reactions: The First Case of Kounis Syndrome Induced by Platelet Transfusion.Vaccines · 2023Article
- The 4G/5G polymorphism of plasminogen activator inhibitor type 1 is a predictor of allergic cough.Frontiers in genetics · 2023Article
- Emerging Roles of Platelets in Allergic Asthma.Frontiers in immunology · 2022Review
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundIt is apparent that the interaction between platelets and eosinophils plays a critical role in the activation of allergic inflammation. We investigated whether blocking of the glycoprotein (GP) IIb/IIIa receptor can attenuate allergic inflammation and airway hyperresponsiveness through inhibition of platelet-eosinophil aggregation (PEA) in asthma.
methodsBALB/c mice were sensitized by intraperitoneal injection of ovalbumin (OVA) on days 0 and 14, followed by 3 nebulized OVA challenges on days 28-30. On each challenge day, 5 mg/kg tirofiban was administered intraperitoneally 30 min before the challenge. Mice were assessed for airway hyperresponsiveness (AHR), airway inflammation, and the degree of PEA. Finally, the activation levels of platelets and eosinophils were evaluated.
resultsTirofiban treatment decreased AHR and eosinophilic inflammation in Bronchoalveolar Lavage (BAL) fluid. This treatment also reduced the levels of interleukin (IL)-4, IL-5, and IL-13 in BAL fluid and airway inflammatory cell infiltration in histological evaluation. Interestingly, the blocking of the GP IIb/IIIa receptor more reduced PEA in both blood and lung tissue of tirofiban-treated mice than in those of the positive control mice, and both eosinophilic and platelet activations were attenuated in tirofiban-treated mice.
conclusionsThe blocking of GP IIb/IIIa receptor with tirofiban can attenuate AHR and airway inflammation through the inhibition of PEA and activation.
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