The blocking effect of the glycoprotein IIb/IIIa receptor in the mouse model of asthma

Abstract Background It is apparent that the interaction between platelets and eosinophils plays a critical role in activation of allergic inflammation. We investigated whether blocking glycoprotein (GP) IIb/IIIa receptor can attenuate inflammation airway hyperresponsiveness through inhibition platelet–eosinophil aggregation (PEA) asthma. Methods BALB/c mice were sensitized by intraperitoneal injection ovalbumin (OVA) on days 0 14, followed 3 nebulized OVA challenges 28–30. On each challenge day, 5 mg/kg tirofiban was administered intraperitoneally 30 min before challenge. Mice assessed for (AHR), inflammation, degree PEA. Finally, levels evaluated. Results Tirofiban treatment decreased AHR eosinophilic Bronchoalveolar Lavage (BAL) fluid. This also reduced interleukin (IL)-4, IL-5, IL-13 BAL fluid inflammatory cell infiltration histological evaluation. Interestingly, GP more PEA both blood lung tissue tirofiban-treated than those positive control mice, platelet activations attenuated mice. Conclusions The with activation.