CELLULAR VACUOLES INDUCED BY HELICOBACTER-PYLORI ORIGINATE FROM LATE ENDOSOMAL COMPARTMENTS

Pathogenic strains of Helicobacter pylori cause progressive vacuolatio n and death of epithelial cells. To identify the nature of vacuoles, t he distribution of markers of various membrane traffic compartments wa s studied. Vacuoles derive from the endocytic pathway since they inclu de the fluid-phase marker Lucifer yellow. Early endosome markers such as rab5, transferrin, and transferrin receptor, as well as the lysosom al hydrolase cathepsin D, are excluded from these structures. In contr ast, the vacuolar membrane is specifically stained by affinity-purifie d antibodies against rab7, a small GTPase, localized to late endosomal compartments. The labeling of rab7 on vacuolar membranes increases as vacuolation progresses, without a concomitant increase of cellular ra b7, Cell vacuolation is inhibited by the microtubule-depolymerizing ag ents nocodazole and colchicine. Taken together, these findings indicat e that the vacuoles specifically originate from late endosomal compart ments.