integrin是ICAM的ligand


所有跟贴·加跟贴·新语丝读书论坛

送交者: 方舟子 于 2008-12-31, 16:08:19:

回答: integrin是受体,ICAMs是ligand 由 trus 于 2008-12-31, 14:16:42:

Am J Physiol Lung Cell Mol Physiol 291: L200-L207, 2006. First published February 3, 2006; doi:10.1152/ajplung.00346.2005

ICAM-1 and LFA-1 play critical roles in LPS-induced neutrophil recruitment into the alveolar space
Abdul Basit,1 Joerg Reutershan,2 Margaret A. Morris,2,3 Michael Solga,4 C. Edward Rose, Jr.,5 and Klaus Ley1,2,3

1Department of Molecular Physiology and Biological Physics, 2Robert M. Berne Cardiovascular Research Center, 3Biomedical Engineering Department, 4Flow Cytometry Core Facility, and 5Division of Pulmonary and Critical Care Medicine, University of Virginia, Charlottesville, Virginia

Submitted 9 August 2005 ; accepted in final form 30 January 2006

Neutrophil recruitment into lung constitutes a major response to airborne endotoxins. In many tissues endothelial intercellular adhesion molecule-1 (ICAM-1) interacts with lymphocyte function associated antigen-1 (LFA-1) on neutrophils, and this interaction plays a critical role in neutrophil recruitment. There are conflicting reports about the role of ICAM-1 in neutrophil recruitment into lungs. We studied neutrophil recruitment into alveolar space in a murine model of aerosolized LPS-induced lung inflammation. LPS induces at least a 100-fold increase in neutrophil numbers in alveolar space, as determined by flow cytometry of bronchoalveolar lavage fluid. Neutrophil recruitment was reduced by 54% in ICAM-1 null mice and by 45% in LFA-1 null mice. In wild-type mice treated with anti-ICAM-1 and anti-LFA-1 antibodies, there was 51 and 58% reduction in the neutrophil recruitment, respectively. In chimeric mice, generated by the transplantation of mixtures of bone marrows from LFA-1 null and wild-type mice, the normalized recruitment of LFA-1 null neutrophils was reduced by 60% compared with wild-type neutrophils. Neither the treatment of ICAM-1 null mice with a function-blocking antibody to LFA-1 nor the treatment of LFA-1 null mice with anti-ICAM-1 antibody resulted in further reduction in the recruitment compared with untreated ICAM-1 null and LFA-1 null mice. We conclude that ICAM-1 and LFA-1 play critical roles in the recruitment of neutrophils into the alveolar space in aerosolized LPS-induced lung inflammation, and LFA-1 serves as a ligand of ICAM-1 in the lung.




所有跟贴:


加跟贴

笔名: 密码: 注册笔名请按这里

标题:

内容: (BBCode使用说明