双歧杆菌粘附体外肠上皮细胞的钙信号传递的研究

本文采用钙荧光探剂 Ｆｌｕｏ—３／ＡＭ染色法，定量研究了双歧杆菌１０２７株、肠致病性大肠杆菌（ＥＰＥＣ）对体外肠上皮细胞Ｌｏｖｏ细胞株粘附的钙信号传递机制。结果表明，双歧杆菌１０２７株粘附可引起Ｌｏｖｏ细胞内Ｃａ~＋２随时间延长而梯度升高，但双歧杆菌１０２７株的作用远不如ＥＰＥＣ明显。同时发现双歧杆菌粘附引起Ｌｏｖｏ。细胞内Ｃａ~２＋升高主要源于细胞外Ｃａ~２＋内流所致，这与ＥＰＥＣ粘附引起宿主细胞内Ｃａ~２＋升高主要源于细胞内Ｃａ~２＋储池的Ｃａ~２＋释放不同。ＥＰＥＣ粘附引起宿主细胞内Ｃａ~２＋大幅度升高是其致病的重要信号传递基础；而双歧杆菌粘附仅引起宿主细胞内Ｃａ~２＋轻度升高，可能是其作为生理性细菌与肠上皮细胞和谐共生的信号传递基础。

AN IN VITRO RESEARCH ON CALCIUM SIGNAL TRANSDUCTION OF INTESTINAL EPITHELIAL CELLS ADHERED WITH BIFIDOBACERIUM 1027 STRAIN

Using calcium florescent probe fluo-3 AM staining method, the authors investigated quantitatively the mechanism of calcium transduction signal of intestinal epithelial cells Lovo colons in vitro adhered by bifidobacterium 1027 strain or enteropathogenic Escherichia coli (EPEC). The results showed that with the adhcsion by bifidobactcrium 1027 strain, the intracellular free calcium level of Lovo cells was elevated time dependently, however the extend was not as evident as those adheded by EPEC. Meanwhile, it was also found that the elevation of intracellular free calcium in Lovo clone adhesed by bifidobaeterium 1027 strain is resulted mainly from extracellular Ca2 influx. This mechanism is totally different from that of elevation of intracellular free calcium in those host cells adhesed by EPEC, which is regarded as a result of the release of Ca2 from intracellular calcium storage pool. A remarkable elevation of intracellular Ca2 in EPEC adhered host cells appears to be a important foundation of the signal transduction of pathogenicity,whereas a slight elevation of Ca2 in host cells adhered by bifidobacteria appears to be the foundation of the signal transduction of benificial and harmonious inteaction between the normal bacterial flora and the intestinal epithelial cells.