Kamiya S, Yamaguchi H, Osaki T, Taguchi H
Department of Microbiology, Kyorin University School of Medicine, Tokyo, Japan.
J Clin Gastroenterol. 1998;27 Suppl 1:S35-9. doi: 10.1097/00004836-199800001-00007.
Among the various virulence factors of Helicobacter pylori the role of its heat shock protein 60 (HSP60, HspB) in mucosal inflammation after H. pylori infection was examined. In flow cytometric analysis, the expression of HSP60 on the cell surface was different, depending on the H. pylori strain used. The HSP60 epitope was also detected on the surface of both human gastric cancer cells (MKN45, KATOIII, and MKN28) and human gastric biopsy specimens. The intensity of the expression of HSP60 on the cell surface correlated significantly with the adhesion of H. pylori to MKN45 cells, but not with urease activity and production of vacuolating cytotoxin. A monoclonal antibody to H. pylori HSP60 inhibited the adhesion of H. pylori to MKN45 cells. These results suggest that HSP60 of H. pylori might act as an important virulence factor after H. pylori infection.
在幽门螺杆菌的各种毒力因子中，研究了其热休克蛋白60（HSP60，HspB）在幽门螺杆菌感染后黏膜炎症中的作用。在流式细胞术分析中，细胞表面HSP60的表达因所用幽门螺杆菌菌株而异。在人胃癌细胞（MKN45、KATOIII和MKN28）以及人胃活检标本的表面也检测到了HSP60表位。细胞表面HSP60的表达强度与幽门螺杆菌对MKN45细胞的黏附显著相关，但与脲酶活性和空泡毒素的产生无关。一种针对幽门螺杆菌HSP60的单克隆抗体可抑制幽门螺杆菌对MKN45细胞的黏附。这些结果表明，幽门螺杆菌的HSP60可能在幽门螺杆菌感染后作为一种重要的毒力因子发挥作用。
