Gustafson C, Kald B, Sjödahl R, Tagesson C
Clinical Research Center, Faculty of Health Sciences, Linköping University, Sweden.
Scand J Gastroenterol. 1991 Oct;26(10):1000-6. doi: 10.3109/00365529109003948.
This study demonstrates the ability of phospholipase C from Clostridium perfringens to stimulate the generation of platelet-activating factor (PAF-acether) in cultured intestinal epithelial cells (INT 407). Cells were exposed to phospholipase C for up to 60 min, and the content of PAF-acether within the cells and in the extracellular medium was determined. Phospholipase C caused a time-dependent formation of PAF-acether within the cells and also release of PAF-acether to the medium. In contrast, phospholipase C did not affect the cellular acetylhydrolase activity or the ability of the cells to metabolize extracellularly added 14C-PAF-acether. These findings suggest the possibility that intestinal epithelial cells, when stimulated with a naturally occurring intestinal bacterial toxin, generate and release PAF-acether. The possibility that this might contribute to the pathophysiology of inflammatory bowel disease is discussed.
本研究证明了产气荚膜梭菌的磷脂酶C刺激培养的肠上皮细胞（INT 407）中血小板活化因子（PAF-乙醚）生成的能力。将细胞暴露于磷脂酶C长达60分钟，并测定细胞内和细胞外培养基中PAF-乙醚的含量。磷脂酶C导致细胞内PAF-乙醚呈时间依赖性形成，并且PAF-乙醚释放到培养基中。相比之下，磷脂酶C不影响细胞乙酰水解酶活性或细胞代谢细胞外添加的14C-PAF-乙醚的能力。这些发现提示了一种可能性，即肠上皮细胞在受到天然存在的肠道细菌毒素刺激时，会生成并释放PAF-乙醚。本文讨论了这可能对炎症性肠病病理生理学产生影响的可能性。
