Open AccessBrefeldin A enhances Helicobacter pylori vacuolating cytotoxin‐induced vacuolation of epithelial cells
Author(s) -
Argent Richard H,
McGarr Christine,
Atherton John C
Publication year - 2004
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2004.tb09692.x
Subject(s) - brefeldin a , vacuole , endosome , microbiology and biotechnology , intracellular , golgi apparatus , lysosome , biogenesis , helicobacter pylori , chemistry , cell culture , biology , cytoplasm , biochemistry , enzyme , genetics , endoplasmic reticulum , gene
Intracellular VacA localises to the vacuolar (late endosome/lysosome) membrane, but little is known about the trafficking of the toxin beyond this region. We show that the Golgi‐disturbing agent brefeldin A (BFA) enhances VacA‐induced vacuolation of epithelial cells by Helicobacter pylori co‐culture and, importantly, BFA treatment induces vacuolation by less toxic forms of VacA. The effect is BFA dose‐dependent and occurs within 2.5 h. These data suggest that VacA may be routed deeper within the cell than the vacuole, and that vacuolation is minimised when this occurs efficiently. This may explain why some forms of VacA do not cause vacuolation and why vacuolation is minimal at the low bacteria:cell ratios observed in vivo.