Background. Adhesion molecules are known to influence postoperative organ function, they are hardly involved in the inflammatory response following the ischemia-reperfusion injury. We sought to investigate the potency of small interfering RNAs to suppress adhesion molecule expression in human pulmonary microvascular endothelial cells. Methods. Human lung microvascular endothelial cells were transfected with specific siRNA followed by a stimulation of the cells with an inflammatory cytokine. Adhesion molecule expression was determined by FACS-analysis, and reduction of intracellular mRNA was determined by qRT-PCR. Furthermore, the attachment of isolated neutrophils on the endothelial layer was determined after siRNA transfection. Results. In summary, siRNA transfection significantly decreased the percentage positive cells in a single cocktail transfection of each adhesion molecule investigated. Adhering neutrophils were diminished as well. Conclusion. siRNA might be a promising tool for the effective suppression of adhesion molecule expression on pulmonary microvascular cells, potentially minimizing leukocyte-endothelial depending interactions of a pulmonary allograft. 1. Introduction Formerly used as an ultimate ratio in end-stage pulmonary diseases, lung transplantation has become a commonly accepted therapy with an increasing number of procedures performed annually. Despite the considerable advantages of perioperative medical care, two main problems remain unresolved: rejection of the graft and primary graft failure (PGF) of the allograft defined by a noncardiogenic pulmonary oedema appearing shortly after reperfusion of the transplanted organ. Large clinical trials report an incidence of between 22% and 57% in patients receiving a lung transplant [1, 2]. A central factor involved in the development of PGF seems to be the expression of adhesion molecules on the surface of pulmonary endothelial cells. They represent a group of different glycoproteins and carbohydrates expressed on the surface of a wide variety of cell types, including endothelial cells. By interfering with receptors on the leukocytes, these adhesion molecules allow initial contact between the leukocytes and the vessel wall. Firm adhesion and transendothelial migration follow, resulting in a sequestration of leukocytes at the endothelium and the later infiltration of the interstitial space. The release of proteolytic enzymes and oxygen-free radicals contributes to damage of the alveolar membrane, resulting in noncardiogenic pulmonary oedema. Furthermore, some adhesion molecules seem to
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