Kleinhans Helge, Kaifi Jussuf T, Mann Oliver, Reinknecht Felix, Freitag Marc, Hansen Bente, Schurr Paulus G, Izbicki Jakob R, Strate Tim G
Department of General-, Visceral- and Thoracic-Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Histol Histopathol. 2009 May;24(5):551-7. doi: 10.14670/HH-24.551.
Inflammatory cytokines have been shown to mediate organ damage by their action on vascular endothelia and leukocytes, in part by upregulating the expression of adhesion molecules, which in turn convey transmigration of leukocytes into tissue. The upregulation and activation of vascular cell adhesion molecules on the endothelial cells avail firm leukocyte adhesion to the vascular endothelium and enhance their transmigration and consecutive tissue injury. The aim of this study was to evaluate the expression of vascular adhesion molecules CD 31 (PECAM-1), CD 106 (VCAM-1), CD 62E (E-Selectin) and CD 62P (P-Selectin) in the pancreas and distant organs of pigs suffering from acute necrotizing pancreatitis (AP). AP was induced in 13 pigs by a combination of intravenous cerulein and intraductal glycodeoxycholic acid. For immunostaining of vascular adhesion molecules slides of porcine pancreas, lung, kidney and liver tissue were stained with monoclonal antibodies (Ab) against PECAM-1-1, VCAM-1 E- and P- SELECTIN. The endothelial cell expression of CD 31 (PECAM-1), CD 106 (VCAM), CD 62E (E-Selectin) and CD 62P (P-SELECTIN) in severe porcine pancreatitis is detectable and upregulation is partly significantly.
炎症细胞因子已被证明可通过作用于血管内皮细胞和白细胞来介导器官损伤，部分原因是上调黏附分子的表达，进而促使白细胞迁移到组织中。内皮细胞上血管细胞黏附分子的上调和激活有助于白细胞牢固黏附于血管内皮，并增强其迁移及随后的组织损伤。本研究的目的是评估急性坏死性胰腺炎（AP）猪的胰腺及远处器官中血管黏附分子CD 31（血小板内皮细胞黏附分子-1）、CD 106（血管细胞黏附分子-1）、CD 62E（E-选择素）和CD 62P（P-选择素）的表达。通过静脉注射雨蛙素和导管内注射甘氨脱氧胆酸联合诱导13头猪发生AP。对于血管黏附分子的免疫染色，猪胰腺、肺、肾和肝组织切片用抗血小板内皮细胞黏附分子-1、血管细胞黏附分子-1、E-选择素和P-选择素的单克隆抗体进行染色。在严重猪胰腺炎中可检测到CD 31（血小板内皮细胞黏附分子-1）、CD 106（血管细胞黏附分子）、CD 62E（E-选择素）和CD 62P（P-选择素）的内皮细胞表达，且部分上调具有显著性。
