4.6 Article

Structural modifications of Helicobacter pylori lipopolysaccharide: An idea for how to live in peace

Journal

WORLD JOURNAL OF GASTROENTEROLOGY
Volume 20, Issue 29, Pages 9882-9897

Publisher

BAISHIDENG PUBLISHING GROUP INC
DOI: 10.3748/wjg.v20.i29.9882

Keywords

Helicobacter pylori; Lipopolysaccharide; Immune response; Adaptation; Inflammation

Funding

  1. Polish Ministry of Science and Higher Education [N401 021 31/0379, N N401 015 136, N N303 451 738, UMO-2013/09/N/NZ6/00805]

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In this review, we discuss the findings and concepts underlying the persistence mechanisms of Helicobacter pylori (H. pylori), a spiral-shaped, Gram-negative rod bacterium that was discovered as a gastric pathogen by Marshall and Warren in 1984. H. pylori colonizes the gastric mucosa of nearly half of the human population. Infections appear in early childhood and, if not treated, persist for life. The presence or absence of symptoms and their severity depend on multiple bacterial components, host susceptibility and environmental factors, which allow H. pylori to switch between pathogenicity and commensalism. Many studies have shown that H. pylori components may facilitate the colonization process and the immune response of the host during the course of H. pylori infection. These H. pylori-driven interactions might result from positive or negative modulation. Among the negative immunomodulators, a prominent position is occupied by a vacuolating toxin A (VacA) and cytotoxin-associated gene A (CagA) protein. However, in light of the recent studies that are presented in this review, it is necessary to enrich this panel with H. pylori lipopolysaccharide (LPS). Together with CagA and VacA, LPS suppresses the elimination of H. pylori bacteria from the gastric mucosa by interfering with the activity of innate and adaptive immune cells, diminishing the inflammatory response, and affecting the adaptive T lymphocyte response, thus facilitating the development of chronic infections. The complex strategy of H. pylori bacteria for survival in the gastric mucosa of the host involves both structural modifications of LPS lipid A to diminish its endotoxic properties and the expression and variation of Lewis determinants, arranged in O-specific chains of H. pylori LPS. By mimicking host components, this phenomenon leaves these bacteria invisible to immune cells. Together, these mechanisms allow H. pylori to survive and live for many years within their hosts. (C) 2014 Baishideng Publishing Group Inc. All rights reserved.

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