Cellular Vacuoles Induced by Helicobacter pylori Originate from Late Endosomal Compartments

Pathogenic strains of Helicobacter pylori cause progressive vacuolation and death of epithelial cells. To identify the nature of vacuoles, the distribution of markers of various membrane traffic compartments was studied. Vacuoles derive from the endocytic pathway since they include the fluid-phase m...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1994-10, Vol.91 (21), p.9720-9724
Main Authors: Papini, E., de Bernard, M., Milia, E., Bugnoli, M., Zerial, M.
Format: Article
Language:English
Subjects:
Adenine - analogs & derivatives
Adenine - pharmacology
Antibodies
Bacteriology
Biomarkers - analysis
Cathepsin D - analysis
Cellular biology
Colchicine - pharmacology
Cytotoxins
Endosomes
Epithelial cells
Fluorescent Antibody Technique
GTP-Binding Proteins - analysis
HeLa Cells
Helicobacter pylori
Helicobacter pylori - pathogenicity
Humans
Immunoblotting
Isoquinolines
Kinetics
Medical research
Nocodazole - pharmacology
Receptors, Transferrin - analysis
Swelling
Toxins
Vacuoles
Vacuoles - drug effects
Vacuoles - metabolism
Vacuoles - ultrastructure
Washing
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Summary:Pathogenic strains of Helicobacter pylori cause progressive vacuolation and death of epithelial cells. To identify the nature of vacuoles, the distribution of markers of various membrane traffic compartments was studied. Vacuoles derive from the endocytic pathway since they include the fluid-phase marker Lucifer yellow. Early endosome markers such as rab5, transferrin, and transferrin receptor, as well as the lysosomal hydrolase cathepsin D, are excluded from these structures. In contrast, the vacuolar membrane is specifically stained by affinity-purified 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 rab7. Cell vacuolation is inhibited by the microtubule-depolymerizing agents nocodazole and colchicine. Taken together, these findings indicate that the vacuoles specifically originate from late endosomal compartments.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.91.21.9720