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.Methods BALB/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.
Highlights
Platelets are well-known primary cells in the hemostasis and tissue repair process, and they are known as effector cells in chronic inflammatory diseases such as asthma [1]
Airway responses to inhaled methylcholine chloride (MCh) were more attenuated and eosinophil counts were more decreased in tirofibantreated mice than in the positive control mice (P < 0.05) (Fig. 1A, B)
The Bronchoalveolar Lavage (BAL) fluid levels of IL-4, IL-5, and IL-13 were more reduced in the tirofiban-treated mice than in the positive control mice (P < 0.01) (Fig. 1)
Summary
Platelets are well-known primary cells in the hemostasis and tissue repair process, and they are known as effector cells in chronic inflammatory diseases such as asthma [1]. The platelet–leukocyte interaction is a fundamental cellular process that is characterized by the exchange of signals between platelets and different types of leukocytes in atherosclerosis and inflammatory reactions. Platelet activation and coagulation abnormalities were found in inflammatory bowel disease patients [10], and the platelet to lymphocyte ratio was correlated with the disease severity of systemic lupus erythematosus patients [11]. These results highlight the potential for the role of platelets in the pathogenesis of inflammatory diseases [12]. We investigated whether blocking of the glycoprotein (GP) IIb/IIIa receptor can attenu‐ ate allergic inflammation and airway hyperresponsiveness through inhibition of platelet–eosinophil aggregation (PEA) in asthma
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