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Mechanisms regulating the selective accumulation of eosinophils in<jats:styled-content style=\"fixed-case\">AEP<\/jats:styled-content>have not been fully established. The objective of this study was to evaluate the mechanisms of eosinophil accumulation in alveolar spaces through examination of bronchoalveolar lavage fluid (<jats:styled-content style=\"fixed-case\">BALF<\/jats:styled-content>) from<jats:styled-content style=\"fixed-case\">AEP<\/jats:styled-content>patients (<jats:styled-content style=\"fixed-case\">AEP\u2010BALF<\/jats:styled-content>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Eosinophils were isolated from the blood of healthy subjects and were placed on a human pulmonary microvascular endothelial cell monolayer cultured on Transwell filters (Coster, Cambridge, MA, USA). A saline control solution or<jats:styled-content style=\"fixed-case\">BALF<\/jats:styled-content>from patients with<jats:styled-content style=\"fixed-case\">AEP<\/jats:styled-content>, sarcoidosis or hypersensitivity pneumonitis was applied to the lower compartment, and the transendothelial migration of the eosinophils was evaluated. The concentrations of cytokines and chemokines in<jats:styled-content style=\"fixed-case\">BALF<\/jats:styled-content>were also measured.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Transmigration of eosinophils across endothelial cells was only induced by the<jats:styled-content style=\"fixed-case\">AEP\u2010BALF<\/jats:styled-content>. This transmigration was blocked by anti\u2010\u03b2<jats:sub>2<\/jats:sub>integrin<jats:styled-content style=\"fixed-case\">mAb<\/jats:styled-content>. The concentrations of eotaxin\u20102 and monocyte chemotactic protein (<jats:styled-content style=\"fixed-case\">MCP<\/jats:styled-content>)\u20104, which are<jats:styled-content style=\"fixed-case\">CC<\/jats:styled-content>chemokine receptor (<jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>) 3 ligands, were elevated in the<jats:styled-content style=\"fixed-case\">AEP\u2010BALF<\/jats:styled-content>, and anti\u2010<jats:styled-content style=\"fixed-case\">CCR3 mAb<\/jats:styled-content>or anti\u2010<jats:styled-content style=\"fixed-case\">MCP<\/jats:styled-content>\u20104<jats:styled-content style=\"fixed-case\">mAb<\/jats:styled-content>inhibited the<jats:styled-content style=\"fixed-case\">AEP\u2010BALF<\/jats:styled-content>\u2010induced transmigration of eosinophils. Furthermore, the concentration of leukotriene (<jats:styled-content style=\"fixed-case\">LT<\/jats:styled-content>)<jats:styled-content style=\"fixed-case\">B<jats:sub>4<\/jats:sub><\/jats:styled-content>was increased in the<jats:styled-content style=\"fixed-case\">AEP\u2010BALF<\/jats:styled-content>, and an<jats:styled-content style=\"fixed-case\">LTB<jats:sub>4<\/jats:sub><\/jats:styled-content>receptor antagonist partially suppressed the<jats:styled-content style=\"fixed-case\">AEP\u2010BALF<\/jats:styled-content>\u2010induced transmigration of eosinophils.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These findings suggest that<jats:styled-content style=\"fixed-case\">CCR3<\/jats:styled-content>ligands including eotaxin\u20102 and<jats:styled-content style=\"fixed-case\">MCP<\/jats:styled-content>\u20104, and<jats:styled-content style=\"fixed-case\">LTB<jats:sub>4<\/jats:sub><\/jats:styled-content>play a role in the accumulation of eosinophils 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