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冷缺血期间细胞间黏附分子-1(ICAM-1)的上调引发人胰腺同种异体移植再灌注时早期中性粒细胞浸润。

Up-regulation of ICAM-1 during cold ischemia triggers early neutrophil infiltration in human pancreas allograft reperfusion.

作者信息

Wiessner R, Eisold S, Linnebacher M, Bünger C, Nizze H, Wacke R, Benz S, Schareck W, Klar E

机构信息

University Hospital Rostock, Rostock, Germany.

出版信息

Transplant Proc. 2009 Nov;41(9):3622-7. doi: 10.1016/j.transproceed.2009.05.039.

DOI:10.1016/j.transproceed.2009.05.039
PMID:19917355
Abstract

BACKGROUND

Graft pancreatitis is induced by ischemia/reperfusion injury in which neutrophil infiltration is believed to be a crucial early event. This observation suggests the presence of adhesion molecules already at the time of reperfusion. Therefore, this study was performed to evaluate the pattern of ICAM-1 and P-Selectin expression on human pancreas allografts following cold ischemia and reperfusion.

PATIENTS AND METHODS

We performed an analysis of pancreas biopsy specimens taken from 13 patients undergoing pancreas transplantation compared with pancreas specimens from 10 patients following resection. Cryostat sections were stained with monoclonal antibodies against CD11b, a neutrophil marker, and the adhesion molecules ICAM-1 and P-Selectin.

RESULTS

Extensive infiltration of CD11b-positive cells was detected in venules and capillaries of pancreas allografts after reperfusion (18.38 +/- 0.87) compared with controls (T1 4.22 +/- 0.55) or with tissue specimens at about 10 hours of cold ischemia (2.60 +/- 0.35; P < .001). Similarly, the pattern of P-Selectin showed a moderate expression before organ harvest (1.54 +/- 0.21) and in samples during cold ischemia (1.46 +/- 0.24) followed by a significantly greater number of P-Selectin-positive cells after reperfusion (2.54 +/- 0.18; P = .005). ICAM-1 was only weakly expressed on the surface of the venular endothelium in all controls (0.77 +/- 0.12). In contrast to P-Selectin, ICAM-1 showed prominent up-regulation during cold ischemia (2.23 +/- 0.23; P < .001) with no further increase after reperfusion (2.23 +/- 0.17).

CONCLUSION

The data suggested that ICAM-1 was already up-regulated during cold ischemia, possibly representing the mechanism of early neutrophil infiltration observed in human pancreatic ischemia/reperfusion injury.

摘要

背景

移植胰腺胰腺炎由缺血/再灌注损伤诱发,其中中性粒细胞浸润被认为是关键的早期事件。这一观察结果表明在再灌注时即已存在黏附分子。因此,本研究旨在评估人胰腺同种异体移植在冷缺血和再灌注后细胞间黏附分子-1(ICAM-1)和P-选择素的表达模式。

患者与方法

我们对13例接受胰腺移植患者的胰腺活检标本进行了分析,并与10例胰腺切除患者的胰腺标本进行比较。冰冻切片用抗中性粒细胞标志物CD11b以及黏附分子ICAM-1和P-选择素的单克隆抗体染色。

结果

与对照组(T1 4.22±0.55)或冷缺血约10小时的组织标本(2.60±0.35;P<.001)相比,再灌注后移植胰腺的小静脉和毛细血管中检测到大量CD11b阳性细胞浸润(18.38±0.87)。同样,P-选择素的表达模式显示在器官获取前(1.54±0.21)和冷缺血期间的样本中(1.46±0.24)呈中度表达,再灌注后P-选择素阳性细胞数量显著增多(2.54±0.18;P = .005)。在所有对照组中,ICAM-1仅在小静脉内皮表面弱表达(0.77±0.12)。与P-选择素不同,ICAM-1在冷缺血期间显著上调(2.23±0.23;P<.001),再灌注后无进一步增加(2.23±0.17)。

结论

数据表明ICAM-1在冷缺血期间即已上调,这可能是人胰腺缺血/再灌注损伤中早期中性粒细胞浸润的机制。

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