Petersen A M, Blom J, Andersen L P, Krogfelt K A
Department of Gastrointestinal Infections and Laboratory for Electron Microscopy, Statens Serum Institsut, Copenhagen, Denmark.
FEMS Immunol Med Microbiol. 2000 Sep;29(1):59-67. doi: 10.1111/j.1574-695X.2000.tb01506.x.
In a human gastric biopsy specimen, 30% of adhering Helicobacter pylori strain AF4 (cagA and VacA positive) was associated with adhesion pedestals. In an AGS cell assay, only a few percent of this type I strain was found to be associated with adhesion pedestals. Nevertheless, a larger proportion of the type I strain was found to invade AGS cells (P < 0.03) and to attach with depressions in the AGS cell membrane (P < 0.03) than a type II strain (cagA and VacA negative). Incubation of AGS cells and H. pylori without adding fetal calf serum (FCS) to the culture medium increased actin accumulations (FITC-phalloidin stained) beneath adhering H. pylori, and decreased H. pylori invasion of AGS cells significantly (P < 0.01). However, no increase in the number of adhesion pedestals was observed by electron microscopy. Proteinase K treatment of FCS eliminated the H. pylori invasion promoting effect (P < 0.01). Our results suggest differences in the ability of H. pylori to induce adhesion pedestals in human gastric epithelial cells and in AGS cells, but a correlation between adhesion pedestal formation in vivo and H. pylori invasion in vitro can be speculated. In addition, H. pylori invasion into AGS cells was found to be mediated by proteins in FCS.
在一份人类胃活检标本中,30%附着的幽门螺杆菌菌株AF4(细胞毒素相关基因A和空泡毒素A呈阳性)与黏附基座有关。在AGS细胞试验中,仅发现百分之几的这种I型菌株与黏附基座有关。然而,与II型菌株(细胞毒素相关基因A和空泡毒素A呈阴性)相比,发现更大比例的I型菌株能够侵入AGS细胞(P<0.03)并附着于AGS细胞膜上的凹陷处(P<0.03)。在培养基中不添加胎牛血清(FCS)培养AGS细胞和幽门螺杆菌,会增加附着的幽门螺杆菌下方的肌动蛋白积累(用异硫氰酸荧光素标记的鬼笔环肽染色),并显著降低幽门螺杆菌对AGS细胞的侵袭(P<0.01)。然而,电子显微镜观察未发现黏附基座数量增加。用蛋白酶K处理胎牛血清可消除幽门螺杆菌的侵袭促进作用(P<0.01)。我们的结果表明,幽门螺杆菌在人胃上皮细胞和AGS细胞中诱导黏附基座的能力存在差异,但可以推测体内黏附基座形成与体外幽门螺杆菌侵袭之间存在相关性。此外,发现幽门螺杆菌对AGS细胞的侵袭是由胎牛血清中的蛋白质介导的。