Seelig R, Seelig H P
Virchows Arch A Pathol Anat Histol. 1976 Aug 19;371(1):69-77. doi: 10.1007/BF00433716.
To study the role of the serum complement system in the early necrosis of acinar cells an acute pancreatitis was produced by injection of basement membrane antibodies into the pancreatic duct of mice and rats. In all animals deposition of complement (C3) and antibasement membrane IgG could be observed in an identical position within areas of acinar cell necrosis. The extent of parenchymal damage and the intensity of complement deposits corresponded to the injected dose of antibodies. The importance of cytolytically active complement components (C5-9) was demonstrated in congenitally C5-defective old line mice which did not show typical centrolobular necroses 1 hr after intraductal injection of antibodies. However, the normocomplementemic mice developed extensive necroses of acinar cells. The results support the hypothesis of a complement-induced acinar cell necrosis in acute pancreatitis.
为研究血清补体系统在腺泡细胞早期坏死中的作用，通过向小鼠和大鼠的胰管注射基底膜抗体来诱发急性胰腺炎。在所有动物中，均可在腺泡细胞坏死区域内的相同位置观察到补体（C3）和抗基底膜IgG的沉积。实质损伤的程度和补体沉积的强度与抗体注射剂量相对应。在先天性C5缺陷的老品系小鼠中证明了溶细胞活性补体成分（C5 - 9）的重要性，这些小鼠在导管内注射抗体1小时后未出现典型的小叶中心坏死。然而，正常补体水平的小鼠出现了广泛的腺泡细胞坏死。这些结果支持了急性胰腺炎中补体诱导腺泡细胞坏死的假说。
