Resolution of Lung Inflammation by CD44

Author:

Teder Priit1,Vandivier R. William2,Jiang Dianhua1,Liang Jiurong1,Cohn Lauren1,Puré Ellen3,Henson Peter M.2,Noble Paul W.1

Affiliation:

1. Department of Medicine, Pulmonary and Critical Care Section, Yale University School of Medicine, New Haven, CT 06520, and VA Connecticut Healthcare System, West Haven, CT 06516, USA.

2. Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206, USA.

3. Wistar Institute, Philadelphia, PA 19104, and The Ludwig Institute for Cancer Research, New York, NY 10158, USA.

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–β 1 . This phenotype was partially reversed by reconstitution with CD44 + cells, thus demonstrating a critical role for this receptor in resolving lung inflammation.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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