Resolution of lung inflammation by CD44
Resolution of lung inflammation by CD44
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DOI：
10.1126/science.1069659
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发表时间：
2002-04-05
期刊：
影响因子：
56.9
通讯作者：
Noble, PW
中科院分区：
文献类型：
--
作者：
Teder, P;Vandivier, RW;Noble, PW
组织损伤和炎症后的成功修复需要炎症反应的解决和细胞外基质分解产物的去除。我们已经研究了细胞表面粘附分子和透明质酸受体CD44是否在解决肺部炎症中起作用。CD44缺陷小鼠在非感染性肺损伤后会出现持续性炎症，其特征是凋亡中性粒细胞清除受损，透明质酸片段在组织损伤部位持续蓄积，转化生长因子β（1）活化受损。这种表型通过与CD44（+）细胞重建而部分逆转，因此证明了这种受体在解决肺部炎症中的关键作用。
Successful repair after tissue injury and inflammation requires resolution of the inflammatory response and removal of extracellular matrix breakdown products. We have examined whether the cell-surface adhesion molecule and hyaluronan receptor CD44 plays a role in resolving lung inflammation. CD44-deficient mice succumb to unremitting inflammation following noninfectious lung injury, characterized by impaired clearance of apoptotic neutrophils, persistent accumulation of hyaluronan fragments at the site of tissue injury, and impaired activation of transforming growth factor-beta(1). This phenotype was partially reversed by reconstitution with CD44(+) cells, thus demonstrating a critical role for this receptor in resolving lung inflammation.