Abstract
Macrolide antibiotics have an anti-inflammatory effect by suppressing lipopolysaccharide-induced IL-8 production. IL-8 secretion from monocytes is observed in Helicobacter pylori infection. Although cag gene products are known to induce IL-8 secretion, whether other bacterial substances can initiate the reaction is not determined. In this study, we show that clarithromycin induced down-regulation of Toll-like receptor 4 expression and did not lead to a decrease in IL-8 production and H. pylori lipopolysaccharide. However, Toll-like receptor 4 activation was possibly not the main cause in the induction of inflammation during H. pylori infection.
MeSH terms
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Anti-Bacterial Agents / pharmacology*
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Clarithromycin / pharmacology*
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Helicobacter Infections / microbiology
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Helicobacter pylori / drug effects
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Helicobacter pylori / immunology
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Helicobacter pylori / metabolism
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Helicobacter pylori / pathogenicity*
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Humans
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Interleukin-8 / biosynthesis*
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Lipopolysaccharides / pharmacology
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Macrolides / pharmacology
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Membrane Glycoproteins / metabolism*
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Monocytes / immunology
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Monocytes / metabolism
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Monocytes / microbiology*
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Receptors, Cell Surface / metabolism*
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Toll-Like Receptor 4
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Toll-Like Receptors
Substances
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Anti-Bacterial Agents
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Interleukin-8
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Lipopolysaccharides
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Macrolides
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Membrane Glycoproteins
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Receptors, Cell Surface
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TLR4 protein, human
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Toll-Like Receptor 4
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Toll-Like Receptors
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Clarithromycin