Resolution of Lung Inflammation by CD44

Priit Teder(VA Connecticut Healthcare System), R. William Vandivier(National Jewish Health), Dianhua Jiang(VA Connecticut Healthcare System), Jiurong Liang(VA Connecticut Healthcare System), Lauren Cohn(VA Connecticut Healthcare System), Ellen Puré(The Wistar Institute), Peter M. Henson(National Jewish Health), Paul W. Noble(VA Connecticut Healthcare System)
Science
April 5, 2002
Cited by 678

Abstract

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-beta1. This phenotype was partially reversed by reconstitution with CD44+ cells, thus demonstrating a critical role for this receptor in resolving lung inflammation.


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