Hypoxia mediates increased neutrophil and macrophage adhesiveness to alveolar epithelial cells

被引:49
作者
Beck-Schimmer, B
Schimmer, RC
Madjdpour, C
Bonvini, JM
Pasch, T
Ward, PA
机构
[1] Univ Zurich, Inst Anesthesiol, Zurich, Switzerland
[2] Univ Zurich, Inst Physiol, Zurich, Switzerland
[3] Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA
[4] Univ Basel, Dept Orthoped Surg, Basel, Switzerland
关键词
D O I
10.1165/ajrcmb.25.6.4433
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Leukocyte infiltration is known to play an important role in hypoxia-induced tissue damage. There is a paucity of information on the role of hypoxia in the expression of adhesion molecules on respiratory epithelial cells. The current studies focus on the adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), their expression pattern on alveolar epithelial cells, and their biologic function under hypoxic conditions. Rat alveolar epithelial cells (AEC) were exposed to hypoxia for several time periods. With 5% oxygen, mRNA for ICAM-1 and VCAM-1 rose by 100%, peaking between 0.5 and 1 h. ICAM-1 and VCAM-1 protein showed an increase between 2 and 4 h. Neutrophil adherence to hypoxia-exposed AEC was enhanced by 115%. This increase was reduced by 83% with anti-ICAM-1 antibody. Adherence of alveolar macrophages to AEC increased by 118% and could be blocked by 95% with anti-VCAM-1 antibody. The present study shows for the first time an early increase of ICAM-1 and VCAM-1 expression on rat AEC under hypoxic conditions. These adhesion molecules are involved in increased adhesiveness of neutrophils and macrophages. Such responses might play an important role in the adhesion of leukocytes and macrophages to lung epithelial cells during hypoxic conditions.
引用
收藏
页码:780 / 787
页数:8
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