Prolonged eosinophil accumulation in allergic lung interstitium of ICAM-2-deficient mice results in extended hyperresponsiveness
Prolonged eosinophil accumulation in allergic lung interstitium of ICAM-2-deficient mice results in extended hyperresponsiveness
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DOI：
10.1016/s1074-7613(00)80002-3
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发表时间：
1999-01-01
期刊：
影响因子：
32.4
通讯作者：
Gutierrez-Ramos, JC
中科院分区：
文献类型：
--
作者：
Gerwin, N;Gonzalo, JA;Gutierrez-Ramos, JC
在过敏性肺炎症的发展过程中，icam -2缺陷小鼠表现出肺间质嗜酸性粒细胞的长期积累，同时气道管腔嗜酸性粒细胞数量的延迟增加。icam -2依赖性肺间质嗜酸性粒细胞的增加和长时间积累导致气道高反应性延长。这些发现揭示了ICAM-2在过敏性肺部疾病的炎症和呼吸成分发展中的重要作用。这种表型是由非造血细胞缺乏ICAM-2表达引起的。内皮细胞上的ICAM-2缺乏导致体外嗜酸性粒细胞迁移减少。ICAM-2对于淋巴细胞归巢或白细胞的发育不是必需的，除了巨核细胞祖细胞，它们明显减少。
ICAM-2-deficient mice exhibit prolonged accumulation of eosinophils in lung interstitium concomitant with a delayed increase in eosinophil numbers in the airway lumen during the development of allergic lung inflammation. The ICAM-2-dependent increased and prolonged accumulation of eosinophils in lung interstitium results in prolonged, heightened airway hyperresponsiveness. These findings reveal an essential role for ICAM-2 in the development of the inflammatory and respiratory components of allergic lung disease. This phenotype is caused by the lack of ICAM-2 expression on non-hematopoietic cells. ICAM-2 deficiency on endothelial cells causes reduced eosinophil transmigration in vitro. ICAM-2 is not essential for lymphocyte homing or the development of leukocytes, with the exception of megakaryocyte progenitors, which are significantly reduced.