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

被引:49
作者
Chmiela, Magdalena [1 ]
Miszczyk, Eliza [1 ]
Rudnicka, Karolina [1 ]
机构
[1] Univ Lodz, Fac Biol & Environm Protect, Dept Immunol & Infect Biol, PL-90237 Lodz, Poland
关键词
Helicobacter pylori; Lipopolysaccharide; Immune response; Adaptation; Inflammation; T-CELL PROLIFERATION; PATTERN-RECOGNITION RECEPTORS; LEWIS ANTIGEN-EXPRESSION; NATURAL-KILLER-CELLS; BLOOD-GROUP ANTIGENS; POTENTIAL ROLE; LIPID-A; MOLECULAR MIMICRY; EXTRACELLULAR-MATRIX; IMMUNE-RESPONSE;
D O I
10.3748/wjg.v20.i29.9882
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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.
引用
收藏
页码:9882 / 9897
页数:16
相关论文
共 143 条
[1]   Bacterial lipopolysaccharides and innate immunity [J].
Alexander, C ;
Rietschel, ET .
JOURNAL OF ENDOTOXIN RESEARCH, 2001, 7 (03) :167-202
[2]   Phagocytosis and persistence of Helicobacter pylori [J].
Allen, Lee-Ann H. .
CELLULAR MICROBIOLOGY, 2007, 9 (04) :817-828
[3]   Helicobacter pylori secreted peptidyl prolyl cis, trans-isomerase drives Th17 inflammation in gastric adenocarcinoma [J].
Amedei, Amedeo ;
Munari, Fabio ;
Della Bella, Chiara ;
Niccolai, Elena ;
Benagiano, Marisa ;
Bencini, Lapo ;
Cianchi, Fabio ;
Farsi, Marco ;
Emmi, Giacomo ;
Zanotti, Giuseppe ;
de Bernard, Marina ;
Kundu, Manikuntala ;
D'Elios, Mario Milco .
INTERNAL AND EMERGENCY MEDICINE, 2014, 9 (03) :303-309
[4]   H pylori and Lewis antigens [J].
Appelmelk, BJ ;
Vandenbroucke-Grauls, CMJE .
GUT, 2000, 47 (01) :10-11
[5]   Cutting edge: Carbohydrate profiling identifies new pathogens that interact with dendritic cell-specific ICAM-3-grabbing nonintegrin on dendritic cells [J].
Appelmelk, BJ ;
van Die, I ;
van Vliet, SJ ;
Vandenbroucke-Grauls, CMJE ;
Geijtenbeek, TBH ;
van Kooyk, Y .
JOURNAL OF IMMUNOLOGY, 2003, 170 (04) :1635-1639
[6]   Molecular mimicry between Helicobacter pylori and the host [J].
Appelmelk, BJ ;
Negrini, R ;
Moran, AP ;
Kuipers, EJ .
TRENDS IN MICROBIOLOGY, 1997, 5 (02) :70-73
[7]   Phase variation in Helicobacter pylori lipopolysaccharide due to changes in the lengths of poly(C) tracts in α3-fucosyltransferase genes [J].
Appelmelk, BJ ;
Martin, SL ;
Monteiro, MA ;
Clayton, CA ;
McColm, AA ;
Zheng, PY ;
Verboom, T ;
Maaskant, JJ ;
Van den Eijnden, DH ;
Hokke, CH ;
Perry, MB ;
Vandenbroucke-Grauls, CMJE ;
Kusters, JG .
INFECTION AND IMMUNITY, 1999, 67 (10) :5361-5366
[8]   Potential role of molecular mimicry between Helicobacter pylori lipopolysaccharide and host Lewis blood group antigens in autoimmunity [J].
Appelmelk, BJ ;
SimoonsSmit, I ;
Negrini, R ;
Moran, AP ;
Aspinall, GO ;
Forte, JG ;
DeVries, T ;
Quan, H ;
Verboom, T ;
Maaskant, JJ ;
Ghiara, P ;
Kuipers, EJ ;
Bloemena, E ;
Tadema, TM ;
Townsend, RR ;
Tyagarajan, K ;
Crothers, JM ;
Monteiro, MA ;
Savio, A ;
DeGraaff, J .
INFECTION AND IMMUNITY, 1996, 64 (06) :2031-2040
[9]  
Bäckhed F, 2003, J INFECT DIS, V187, P829
[10]   MOLECULAR-STRUCTURES THAT INFLUENCE THE IMMUNOMODULATORY PROPERTIES OF THE LIPID-A AND INNER-CORE REGION OLIGOSACCHARIDES OF BACTERIAL LIPOPOLYSACCHARIDES [J].
BAKER, PJ ;
HRABA, T ;
TAYLOR, CE ;
STASHAK, PW ;
FAUNTLEROY, MB ;
ZAHRINGER, U ;
TAKAYAMA, K ;
SIEVERT, TR ;
HRONOWSKI, XP ;
COTTER, RJ ;
PEREZPEREZ, G .
INFECTION AND IMMUNITY, 1994, 62 (06) :2257-2269