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Virulence Mechanisms and Persistence Strategies of the Human Gastric Pathogen Helicobacter pylori

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Molecular Mechanisms of Bacterial Infection via the Gut

Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 337))

Abstract

The human gastric pathogen Helicobacter pylori is able to establish an infection in a hostile environment with virtually no competitors. For this purpose, it has elaborated a set of colonization factors which facilitate both survival under acid exposure, motility and orientation in a highly viscous mucus layer, and adherence to epithelial surfaces. A more intimate interaction with gastric epithelia provides the basis to influence gene expression profiles as well as morphological transitions via signaling cascades or via direct activities of virulence factors. H. pylori is also one of the most genetically diverse of organisms, and variations are not only found in outer membrane adhesins, but also in two major virulence factors, the VacA cytotoxin and the cag pathogenicity island. Both factors are able to target different cell types and different interaction partners to induce a wide range of possible cellular effects. Despite the fact that H. pylori elicits a strong inflammatory response, the immune system fails to clear the infection, suggesting that immune evasion strategies are used. The mechanisms for immune evasion include the induction of a strongly polarized immune response, a modulation of phagocytosis and neutrophil function, and an inhibition of lymphocyte proliferation. Prolonged inflammation and direct action of bacterial factors may lead to impairment of gland function and eventually to carcinogenesis.

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Abbreviations

DC-SIGN:

Dendritic cell-specific ICAM-3-grabbing nonintegrin

EGFR:

Epidermal growth factor receptor

FAK:

Focal adhesion kinase

GSK:

Glycogen synthase kinase

IL:

Interleukin

iNOS:

Inducible nitric oxide synthase

JNK:

Jun N-terminal kinase

Leb :

Lewis b

LPS:

Lipopolysaccharide

MALT:

Mucosa-associated lymphoid tissue

MMP:

Matrix metalloproteinase

NFAT:

Nuclear factor of activated T cells

PAI:

Pathogenicity island

PI3K:

Phosphatidylinositol-3-kinase

PKC:

Protein kinase C

PMA:

Phorbol-myristate-acetate

PMN:

Polymorphonuclear cell

ROS:

Reactive oxygen species

sLex :

Sialyl-Lewis x

T4SS:

Type IV secretion system

TLR:

Toll-like receptor

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Acknowledgements

The authors would like to thank Werner Goebel and Xaver Sewald for critical comments on the manuscript. We apologize to all authors whose work could not be cited due to space limitations. Work in the authors’ laboratory is supported by grants from the Deutsche Forschungsgemeinschaft (SFB576, project B1; HA2697/10-1) and from the Federal Ministry of Education and Research (ERA-NET Pathogenomics, HELDIVNET) to R.H.

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Fischer, W., Prassl, S., Haas, R. (2009). Virulence Mechanisms and Persistence Strategies of the Human Gastric Pathogen Helicobacter pylori . In: Sasakawa, C. (eds) Molecular Mechanisms of Bacterial Infection via the Gut. Current Topics in Microbiology and Immunology, vol 337. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-01846-6_5

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