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DNA Transfer and Toll-like Receptor Modulation by Helicobacter pylori

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Molecular Pathogenesis and Signal Transduction by Helicobacter pylori

Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 400))

Abstract

Helicobacter pylori is the most common bacterial infection worldwide, and virtually all infected persons develop co-existing gastritis. H. pylori is able to send and receive signals from the gastric mucosa, which enables both host and microbe to engage in a dynamic equilibrium. In order to persist within the human host, H. pylori has adopted dichotomous strategies to both induce inflammation as a means of liberating nutrients while simultaneously tempering the immune response to augment its survival. Toll-like receptors (TLRs) and Nod proteins are innate immune receptors that are present in epithelial cells and represent the first line of defense against pathogens. To ensure persistence, H. pylori manipulates TLR-mediated defenses using strategies that include rendering its LPS and flagellin to be non-stimulatory to TLR4 and TLR5, respectively; translocating peptidoglycan into host cells to induce NOD1-mediated anti-inflammatory responses; and translocating DNA into host cells to induce TLR9 activation.

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Acknowledgements

We would like to acknowledge Drs. Carrie Shaffer and Maria Hadjifrangiskou for providing the confocal micrograph.

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Correspondence to Richard M. Peek .

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Varga, M.G., Peek, R.M. (2017). DNA Transfer and Toll-like Receptor Modulation by Helicobacter pylori . In: Tegtmeyer, N., Backert, S. (eds) Molecular Pathogenesis and Signal Transduction by Helicobacter pylori. Current Topics in Microbiology and Immunology, vol 400. Springer, Cham. https://doi.org/10.1007/978-3-319-50520-6_8

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