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Helicobacter. 2017 Sep;22 Suppl 1. doi: 10.1111/hel.12405.

Pathogenesis of Helicobacter pylori infection.

Author information

1
Pasteur Institute, Department of Microbiology, Helicobacter Pathogenesis Unit, Paris Cedex 15, France.
2
INSERM U1173, Faculty of Health Sciences Simone Veil, Université Versailles-Saint-Quentin, Saint Quentin en Yvelines, France.
3
Graduate School of Medicine and Pharmaceutical Sciences, Department of Gastroenterology, University of Toyama, Sugitani, Toyama, Japan.

Abstract

Helicobacter pylori is responsible for the most commonly found infection in the world's population. It is the major risk factor for gastric cancer development. Numerous studies published over the last year provide new insights into the strategies employed by H. pylori to adapt to the extreme acidic conditions of the gastric environment, to establish persistent infection and to deregulate host functions, leading to gastric pathogenesis and cancer. In this review, we report recent data on the mechanisms involved in chemotaxis, on the essential role of nickel in acid resistance and gastric colonization, on the importance of adhesins and Hop proteins and on the role of CagPAI-components and CagA. Among the host functions, a special focus has been made on the escape from immune response, the ability of bacteria to induce genetic instability and modulate telomeres, the mechanism of autophagy and the deregulation of micro RNAs.

KEYWORDS:

Type IV secretion system; acid resistance; adhesins; autophagy; chemotaxis; microRNA

PMID:
28891130
DOI:
10.1111/hel.12405
[Indexed for MEDLINE]

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