@article {Vanderstockenp4110, author = {G. Vanderstocken and B. Bondue and M. Horckmans and L. Di Pietrantonio and B. Robaye and J.M. Boeynaems and D. Communi}, title = {LSC 2011 Abstract: P2Y2 receptor regulates VCAM-1 membrane and soluble forms and eosinophil accumulation during lung inflammation}, volume = {38}, number = {Suppl 55}, elocation-id = {p4110}, year = {2011}, publisher = {European Respiratory Society}, abstract = {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.}, issn = {0903-1936}, URL = {https://erj.ersjournals.com/content/38/Suppl_55/p4110}, eprint = {https://erj.ersjournals.com/content}, journal = {European Respiratory Journal} }