Journal
JOURNAL OF IMMUNOLOGY
Volume 185, Issue 6, Pages 3702-3707Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0903908
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Funding
- French Community of Belgium, Prime Minister's Office, Federal Service for Science, Technology and Culture
- Fund of Scientific and Medical Research
- Emile DEFAY Fund
- Walloon Region (Programme of Excellence)
- European Community [LSHB-2003-503337]
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ATP has been defined as a key mediator of asthma. In this study, we evaluated lung inflammation in mice deficient for the P2Y(2) purinergic receptor. We observed that eosinophil accumulation, a distinctive feature of lung allergic inflammation, was defective in OVA-treated P2Y(2)-deficient mice compared with OVA-treated wild type animals. Interestingly, the upregulation of VCAM-1 was lower on lung endothelial cells of OVA-treated P2Y(2)(-/-) 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 P2Y(2)-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 P2Y(2)-deficient mice. In contrast, we observed comparable infiltration of macrophages and neutrophils in the BALF of LPS-aerosolized P2Y(2)(+/+) and P2Y(2)(-/-) 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 P2Y(2) as a regulator of membrane and soluble forms of VCAM-1 and eosinophil accumulation during lung inflammation. The Journal of Immunology, 2010, 185: 3702-3707.
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