We have demonstrated that clinical isolates of Helicobacter pylori pre
ferentially bind to sulfatides ((ISO3)-S-3-GalCer) and GM(3) gangliosi
des (II(3)NeuAcLacCer), two predominant acidic glycosphingolipids in t
he human gastric mucosa, on thin-layer chromatography plates, However,
it has not Set been clarified that these glycosphingolipids truly ser
ve as adhesion receptors for H. pylori in live cells. In this study, w
e used a gastric cancer cell line, KATO III, as a cellular model of H.
pylori adhesion and examined the role of sulfatides in attachment. Th
e adhesion of H. pylori (i.e,, a standard strain of H, pylori, NCTC 11
637) to KATO III cells and the effects of various substances on this a
dhesion were monitored and semiquantitated by flow cytometric analysis
, Sulfated glycoconjugates, such as heparin and gastric mucin, signifi
cantly inhibited H, pylori adhesion to KATO III cells, Membrane prepar
ations from KATO III cells strongly inhibited this adhesion, In the me
mbrane preparations, sulfatides were present as a major acidic glycosp
hingolipid, With the exception of sulfatides, no distinct adhesion of
H, pylori to glycosphingolipids from KATO III cells was observed, More
over, H, pylori did not bind to any membrane proteins of KATO III cell
s, Finally, a monoclonal anti-sulfatide antibody markedly reduced H, p
ylori adhesion to KATO III cells, These results suggest that sulfatide
s, and possibly related sulfated compounds, serve as a major receptor
for cell adhesion by H. pylori.