Resistance of primary murine CD4+ T cells to Helicobacter pylori vacuolating cytotoxin.

Algood HM, Torres VJ, Unutmaz D, Cover TL
Infect Immun. 2007 75 (1): 334-41

PMID: 17074854 · PMCID: PMC1828377 · DOI:10.1128/IAI.01063-06

Persistent colonization of the human stomach by Helicobacter pylori is a risk factor for the development of gastric cancer and peptic ulcer disease. H. pylori secretes a toxin, VacA, that targets human gastric epithelial cells and T lymphocytes and enhances the ability of H. pylori to colonize the stomach in a mouse model. To examine how VacA contributes to H. pylori colonization of the mouse stomach, we investigated whether murine T lymphocytes were susceptible to VacA activity. VacA inhibited interleukin-2 (IL-2) production by a murine T-cell line (LBRM-33), similar to its effects on a human T-cell line (Jurkat), but did not inhibit IL-2 production by primary murine splenocytes or CD4+ T cells. VacA inhibited activation-induced proliferation of primary human CD4+ T cells but did not inhibit the proliferation of primary murine CD4+ T cells. Flow cytometry studies indicated that the levels of VacA binding to primary murine CD4+ T cells were significantly lower than levels of VacA binding to human CD4+ T cells. This suggests that the resistance of primary murine CD4+ T cells to VacA is attributable, at least in part, to impaired VacA binding to these cells.

MeSH Terms (15)

Animals Bacterial Proteins CD4-Positive T-Lymphocytes Cell Proliferation Cells, Cultured Flow Cytometry Helicobacter Infections Helicobacter pylori Humans Immunoblotting Interleukin-2 Jurkat Cells Lymphocyte Activation Mice p38 Mitogen-Activated Protein Kinases

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