TY - JOUR T1 - LSC 2011 Abstract: P2Y2 receptor regulates VCAM-1 membrane and soluble forms and eosinophil accumulation during lung inflammation JF - European Respiratory Journal JO - Eur Respir J VL - 38 IS - Suppl 55 SP - p4110 AU - G. Vanderstocken AU - B. Bondue AU - M. Horckmans AU - L. Di Pietrantonio AU - B. Robaye AU - J.M. Boeynaems AU - D. Communi Y1 - 2011/09/01 UR - http://erj.ersjournals.com/content/38/Suppl_55/p4110.abstract N2 - ATP has been defined as a key mediator of asthma. In this study, we evaluated lung inflammation in mice deficient for the P2Y2 purinergic receptor. We observed that eosinophil accumulation, a distinctive feature of lung allergic inflammation, was defective in OVA-treated P2Y2-deficient mice compared with OVA-treated wild type animals. Interestingly, the upregulation of VCAM-1 was lower on lung endothelial cells of OVA-treated P2Y2-/- mice compared with OVA-treated wild type animals. Adhesion assays demonstrated that the action of UTP on leukocyte adhesion through the regulation of endothelial VCAM-1 was abolished in P2Y2-deficient lung endothelial cells. Additionally, the level of soluble VCAM-1, reported as an inducer of eosinophil chemotaxis, was strongly reduced in the bronchoalveolar lavage fluid (BALF) of P2Y2-deficient mice. In contrast, we observed comparable infiltration of macrophages and neutrophils in the BALF of LPS-aerosolized P2Y2+/+ and P2Y2-/- mice. This difference could be related to the much lower level of ATP in the BALF of LPS-treated mice compared with OVA-treated mice.Our data define P2Y2 as a regulator of membrane and soluble forms of VCAM-1 and eosinophil accumulation during lung inflammation. ER -