Abstract
Stx1 and Stx2 produced by Shiga toxin-producing Escherichia coli are cytotoxic due to their N-glycosidase activity on 28S rRNA. In this study, we have shown that proinflammatory cytokine mRNAs, especially IL-8, were induced by Stx1 and Stx2 in Caco-2 cells. A non-toxic mutant of Stxl which lacks N-glycosidase activity did not induce cytokine mRNAs. IL-8 production at the protein level was enhanced by Stx1 and Stx2, but not by the mutant Stx1. These results demonstrate that Shiga toxins induce expression and synthesis of cytokines in Caco-2 cells and their N-glycosidase activity is essential for the induction.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Substitution
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Bacterial Toxins / genetics
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Bacterial Toxins / metabolism
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Bacterial Toxins / pharmacology*
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Bacterial Toxins / toxicity
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Binding Sites
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Caco-2 Cells
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Chemokine CCL2 / genetics
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Chemokine CCL4
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Cytokines / biosynthesis
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Cytokines / genetics*
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Enzyme-Linked Immunosorbent Assay
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Escherichia coli / genetics
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Gene Expression Regulation / drug effects
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Glycoside Hydrolases / genetics
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Glycoside Hydrolases / metabolism*
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Glycoside Hydrolases / pharmacology
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Humans
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Interleukin-8 / biosynthesis
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Interleukin-8 / genetics
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Macrophage Inflammatory Proteins / genetics
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Mutation*
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Protein Biosynthesis
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Recombinant Proteins / genetics
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Recombinant Proteins / metabolism
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Recombinant Proteins / pharmacology
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Reverse Transcriptase Polymerase Chain Reaction
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Shiga Toxins
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Shigella / enzymology*
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Trihexosylceramides / metabolism
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Tumor Necrosis Factor-alpha / genetics
Substances
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Bacterial Toxins
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Chemokine CCL2
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Chemokine CCL4
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Cytokines
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Interleukin-8
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Macrophage Inflammatory Proteins
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Recombinant Proteins
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Shiga Toxins
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Trihexosylceramides
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Tumor Necrosis Factor-alpha
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globotriaosylceramide
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Glycoside Hydrolases