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Salmonella typhimurium induces an inositol phosphate flux in infected epithelial cells
Author(s) -
Ruschkowski S.,
Rosenshine I.,
Finlay B. Brett
Publication year - 1992
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.1574-6968.1992.tb05353.x
Subject(s) - salmonella , inositol , microbiology and biotechnology , inositol phosphate , enterobacteriaceae , flux (metallurgy) , chemistry , phosphate , bacteria , biology , escherichia coli , biochemistry , receptor , gene , genetics , organic chemistry
Salmonella typhimurium , like many other intracellular pathogens, is capable of inducing its own uptake into non‐phagocytic cells by a process termed invasion, and residing within a membrane‐bound inclusion. During invasion it causes significant rearrangment of the host cytoskeleton, indicating that signals are transduced between the bacterium and the host cell cytoplasm, across the eukaryotic cell membrane. We found that intracellular inositol phosphate concentrations in HeLa cells increased during S. typhimurium entry and returned to normal levels after bacterial internalization. A chelator of intracellular calcium (BAPTA / AM) blocked S. typhimurium uptake into HeLa epithelial cells, but extracellular calcium chelators (BAPTA, EGTA, EDTA) had no effect on bacterial invasion. These results indicate that S. typhimurium may activate host cell phospholipase C activity to form inositol phosphates which in turn stimulate release of intracellular calcium stores to facilitate bacterial uptake.

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