Role of sulfatides in adhesion of Helicobacter pylori to gastric cancer cells.
We have demonstrated that clinical isolates of Helicobacter pylori preferentially bind to sulfatides (I3SO3-GalCer) and GM3 gangliosides (II3NeuAcLacCer), two predominant acidic glycosphingolipids in the human gastric mucosa, on thin-layer chromatography plates. However, it has not yet been clarified that these glycospingolipids truly serve as adhesion receptors for H. pylori in live cells. In this study, we used a gastric cancer cell line, KATO III, as a cellular model of H. pylori adhesion and examined the role of sulfatides in attachment. The adhesion of H. pylori (i.e., a standard strain of H. pylori, NCTC 11637) to KATO III cells and the effects of various substances on this adhesion were monitored and semiquantitated by flow cytometric analysis. Sulfated glycoconjugates, such as heparin and gastric mucin, significantly inhibited H. pylori adhesion to KATO III cells. Membrane preparations from KATO III cells strongly inhibited this adhesion. In the membrane preparations, sulfatides were present as a major acidic glycosphinoglipid. With the exception of sulfatides, no distinct adhesion of H. pylori to glycospingolipids from KATO III cells were observed. Moreover, H. pylori did not bind to any membrane proteins of KATO III cells. Finally, a monoclonal anti-sulfatide antibody markedly reduced H. pylori adhesion to KATO III cells. These results suggest that sulfatides, and possibly related sulfated compounds, serve as a major receptor for cell adhesion by H. pylori.
Third Department of Internal Medicine, University of Tokyo, Japan.
S
S
Kamisago
M
M
Iwamori
T
T
Tai
K
K
Mitamura
Y
Y
Yazaki
K
K
Sugano
D001422:Bacterial Adhesion; D006028:Glycosphingolipids / Q000378:metabolism; D016480:Helicobacter pylori / Q000502:physiology*; D006801:Humans; D013274:Stomach Neoplasms / Q000382:microbiology*; D013433:Sulfoglycosphingolipids / Q000378:metabolism*; D014407:Tumor Cells, Cultured
D006028:Glycosphingolipids; D013433:Sulfoglycosphingolipids