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World J Gastroenterol. Aug 7, 2014; 20(29): 9882-9897
Published online Aug 7, 2014. doi: 10.3748/wjg.v20.i29.9882
Structural modifications of Helicobacter pylori lipopolysaccharide: An idea for how to live in peace
Magdalena Chmiela, Eliza Miszczyk, Karolina Rudnicka
Magdalena Chmiela, Eliza Miszczyk, Karolina Rudnicka, Department of Immunology and Infectious Biology, Faculty of Biology and Environmental Protection, University of Łódź, 90-237 Łódź, Poland
Author contributions: Chmiela M designed and wrote the manuscript; Rudnicka K wrote the manuscript and prepared the figures; Miszczyk E collected and prepared literature.
Supported by Certain results presented in this review derived from studies that were supported by the Polish Ministry of Science and Higher Education grants, N401 021 31/0379, N N401 015 136, N N303 451 738 and UMO-2013/09/N/NZ6/ 00805
Correspondence to: Magdalena Chmiela, Professor, Department of Immunology and Infectious Biology, Faculty of Biology and Environmental Protection, University of Łódź, Banacha 12/16, 90-237 Łódź, Poland.
Telephone: +48-42-6354186 Fax: +48-42-6655818
Received: September 26, 2013
Revised: February 21, 2014
Accepted: April 21, 2014
Published online: August 7, 2014

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.

Keywords: Helicobacter pylori, Lipopolysaccharide, Immune response, Adaptation, Inflammation

Core tip:Helicobacter pylori (H. pylori), a Gram-negative bacterium, colonizes the gastric mucosa of at least half of the human population and possesses a unique lipopolysaccharide (LPS) structure. According to recent studies, this structure contributes to the immunomodulatory properties of LPS. The structural rearrangements of H. pylori LPS, especially in relation to the lipid A and O side chains, result in a unique pattern of interactions between the bacterium and the host. In this review, we report and discuss the actual findings underlying the LPS-driven “persistence mechanisms” of H. pylori, explaining how structural modifications may allow these bacteria to “live in peace” within a human host.