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Am J Physiol Lung Cell Mol Physiol (February 1, 2002). doi:10.1152/ajplung.00433.2001
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Articles in PresS, published online ahead of print February 1, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00433.2001
Submitted on November 5, 2001
Accepted on January 18, 2002

Phosphodiesterase type 4 inhibitor reduces the retention of polymorphonuclear leukocytes in the lung

Yukio Sato1*, Shyoko Sato1, Tatsuo Yamamoto1, Shigemi Ishikawa1, Masataka Onizuka1, and Yuzuru Sakakibara1

1 Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Japan

* To whom correspondence should be addressed. E-mail: ysato{at}md.tsukuba.ac.jp.

Phosphodiesterase (PDE) type 4 is the predominant PDE isozyme in polymorphonuclear leukocyte (PMN) and plays a key role in the regulation of PMN activation. The aim of this study was to examine the effect of a PDE type 4 inhibitor, rolipram, on the functional changes and the retention of PMN in the lung. In vitro, F-actin content, L-selectin and CD11b expression of PMN stimulated by FMLP were measured using flow cytometry. PMN deformability was evaluated using silicon microchannel. Rolipram reduced the increase of F-actin and CD11b, but did not change the decrease of L-selectin. Rolipram inhibited the increase of the transit time of PMN through the microchannel. In vivo, the retention of PMN in the lung was evaluated by infusing labeled blood into Vena Cava and examining the recovery into aortic root samples in rabbits. Rolipram inhibited the retention of stimulated PMN in the lung. In conclusion, a PDE type 4 inhibitor, rolipram, reduces the retention of PMN in the lung by reducing deformability change and CD11b up-regulation of PMN.




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