Salmonella typhimurium induces an inositol phosphate flux in infected epithelial cells

S. Ruschkowski, I. Rosenshine, B. Brett Finlay*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

71 Scopus citations


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.

Original languageAmerican English
Pages (from-to)121-126
Number of pages6
JournalFEMS Microbiology Letters
Issue number2-3
StatePublished - 15 Aug 1992
Externally publishedYes

Bibliographical note

Funding Information:
We would like to thank M. Gold for helpful discussions about measuring 1P production. This work was supported by the Medical Research Council of Canada. B.B.F. is a recipient of an International Research Scholars Award from the Howard Hughes Medical Institute, and I.R. is supported by a long term fellowship from the European Molecular Biology Organization (EMBO).


  • Inositol phosphate
  • Invasion
  • Salmonella typhimurium
  • Signal transduction


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