Identification of a
 <scp>d</scp>
 -
 glycero
 -
 <scp>d</scp>
 -
 manno
 -Heptosyltransferase Gene from
 Helicobacter pylori

Hiratsuka, Koji; Logan, Susan M.; Conlan, J. Wayne; Chandan, Vandana; Aubry, Annie; Smirnova, N. I.; Ulrichsen, Heather; Chan, Kalok; Griffith, Douglas W.; Harrison, Blair A.; Li, Jianjun; Altman, Eleonora

doi:10.1128/jb.187.15.5156-5165.2005

Cited by 38 publications

(48 citation statements)

References 60 publications

(65 reference statements)

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“…The outer core structure of H . pylori 26695 LPS was initially postulated to contain a DD-heptan with the first DD-Hep residue connecting a side-branched α-1,6-glucan [6,16,17,19–22], but a recent reinvestigation into the structure of 26695 LPS revised the outer core as being a linear arrangement of DD-heptan and α-1,6-glucan linked to the inner core through a trisaccharide (GlcNAc-Fuc-DD-Hep) termed as Trio [15] ( Fig 1A ). Furthermore, the attachment site of the O-antigen to the core-oligosaccharide has not been identified [13,15], and therefore the precise assignment of the O-antigen and core-oligosaccharide domains remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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The redefinition of Helicobacter pylori lipopolysaccharide O-antigen and core-oligosaccharide domains

Yang

Liao

et al. 2017

PLoS Pathog

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Helicobacter pylori lipopolysaccharide promotes chronic gastric colonisation through O-antigen host mimicry and resistance to mucosal antimicrobial peptides mediated primarily by modifications of the lipid A. The structural organisation of the core and O-antigen domains of H. pylori lipopolysaccharide remains unclear, as the O-antigen attachment site has still to be identified experimentally. Here, structural investigations of lipopolysaccharides purified from two wild-type strains and the O-antigen ligase mutant revealed that the H. pylori core-oligosaccharide domain is a short conserved hexasaccharide (Glc-Gal-DD-Hep-LD-Hep-LD-Hep-KDO) decorated with the O-antigen domain encompassing a conserved trisaccharide (-DD-Hep-Fuc-GlcNAc-) and variable glucan, heptan and Lewis antigens. Furthermore, the putative heptosyltransferase HP1284 was found to be required for the transfer of the third heptose residue to the core-oligosaccharide. Interestingly, mutation of HP1284 did not affect the ligation of the O-antigen and resulted in the attachment of the O-antigen onto an incomplete core-oligosaccharide missing the third heptose and the adjoining Glc-Gal residues. Mutants deficient in either HP1284 or O-antigen ligase displayed a moderate increase in susceptibility to polymyxin B but were unable to colonise the mouse gastric mucosa. Finally, mapping mutagenesis and colonisation data of previous studies onto the redefined organisation of H. pylori lipopolysaccharide revealed that only the conserved motifs were essential for colonisation. In conclusion, H. pylori lipopolysaccharide is missing the canonical inner and outer core organisation. Instead it displays a short core and a longer O-antigen encompassing residues previously assigned as the outer core domain. The redefinition of H. pylori lipopolysaccharide domains warrants future studies to dissect the role of each domain in host-pathogen interactions. Also enzymes involved in the assembly of the conserved core structure, such as HP1284, could be attractive targets for the design of new therapeutic agents for managing persistent H. pylori infection causing peptic ulcers and gastric cancer.

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Section: Introductionmentioning

confidence: 99%

“…pylori LPS performed by the research groups of Trent [9,18,23–28], Moran [29–31], Altman [15,19,22,32–35] and Feldman [36,37], the goal of this study was to precisely define the core-oligosaccharide and O-antigen domains. The LPS of the H .…”

Section: Introductionmentioning

confidence: 99%

The redefinition of Helicobacter pylori lipopolysaccharide O-antigen and core-oligosaccharide domains

Yang

Liao

et al. 2017

PLoS Pathog

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“…H. pylori strain SS1 was from Dr. A. Lee (University of New South Wales, Sydney, Australia). Cells were grown at 37°C on antibiotic-supplemented Columbia Blood agar (Difco) plates containing 7% horse blood in microaerophilic environment for 72 h as previously described ( 23 ). Kanamycin (10 mg/l) was used for mutant strains in addition to regular antibiotics ( 23 ).…”

Section: Bacterial Strains and Growth Conditionsmentioning

confidence: 99%

Microwave-assisted sample preparation for rapid and sensitive analysis of H. pylori lipid A applicable to a single colony

Zhou

Chandan

Liu

et al. 2009

Journal of Lipid Research

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This article is available online at http://www.jlr.org of H. pylori outer membrane. The H. pylori LPS consists of a lipid A region, a core region, and an O-chain polysaccharide (also known as the O-antigen) ( 3 ). Lipid A, the hydrophobic moiety of LPS and a glucosamine-based saccharolipid, is the principal structural component responsible for the range of biological activities of LPS ( 4, 5 ).Generally, lipid A is a glucosamine disaccharide that carries phosphates at positions 1 and 4 ′ and usually has four primary (glucosamine-linked) hydroxyacyl chains and one or more secondary acyl chains ( 3, 6, 7 ). However, H. pylori lipid A is different from that of other bacterial species, including both phosphorylation and acylation patterns ( 8 ). The lipid A of H. pylori contains a phosphoethanolamine ( P Etn) group directly linked to the 1-position of the disaccharide backbone. This is in contrast to the P Etn groups found in other pathogenic Gram-negative bacteria, which are attached to the lipid A phosphate group to form a pyrophosphate linkage ( 9, 10 ). In addition, the predominant absence of ester-bound 4'-phosphate and the presence of tetraacyl lipid A with fatty acids of 16 to 18 carbons in length differentiate H. pylori lipid A from that of other Gram-negative bacteria. H. pylori synthesizes two types of lipid A molecules: hexaacyl-and tetraacyl-lipid A. Hexaacyllipid A has two phosphates or phosphoethanolamines on the lipid A disaccharide backbone, whereas tetraacyllipid A contains only one phosphate ( 8 ). It has also been reported that H. pylori does not survive long before it is deacylated at the 3 ′ position from hexaacyl structure to form the tetraacyl major lipid A species ( 11 ). The toxicity of H. pylori tetraacyl-lipid A on human monocytes is ‫ف‬ 4-fold lower than that of the hexaacyl form ( 12 ). It has been suggested that the phosphorylation and acylation patterns in lipid A of H. pylori LPS are responsible for its low biological activity ( 13,14 ).

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Section: Determination Of Minimum Inhibitory Concentration (Mic)mentioning

confidence: 99%

“…The acidified-WCC was centrifuged at 4,100 × g for 1 min in order to remove the insoluble substances formed by acidification, and was then kept at 4℃ (Trang et al, 2009). In addition, 4 strains frequently seen world-wide, NCTC11637 (derived from USA), SS1 (derived from Australia) (Hiratsuka et al, 2005), J99 (derived from USA) (Hiratsuka et al, 2005) and 26695 (derived from United Kingdom) (Kidd et al, 2001;Akopyants et al, 1998), were employed in this study.All H. pylori strains were grown on Brucella agar plates supplemented with 10% horse serum (HS) and 1.4% agar at 37℃ under microaerobic conditions (10% CO 2 ) (Sanyo CO 2 incubator, Osaka, Japan) for 48 h, as described previously (Trang et al, 2009). Brucella medium supplemented with 10% HS (Brucella-serum medium) was used, unless otherwise stated.…”

mentioning

confidence: 99%

In Vitro Anti-Helicobacter pylori Activity of Chinese Chive (Allium tuberosum)

Kudo

Takeuchi

Shimamura

et al. 2011

FSTR

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The anti-Helicobacter pylori (H. pylori) activity of a water extract of Chinese chive (Allium tuberosum) (WCC) was investigated. On disk diffusion assay, WCC effectively inhibited the growth of all 21 strains tested, including isogenic mutants, showing inhibition diameters of 12 to 29 mm, irrespective of drug susceptibility and clinical manifestation. The minimum inhibitory concentration (MIC) of WCC was 2.45 mg dry weight/mL. Killing assay with multiples of MIC confirmed that WCC had bactericidal activity and that the inhibitory effects were dose dependent. In addition, to determine whether the inhibitory activity of WCC under severe stress conditions, such as heat and acidity, is altered, the stability of WCC was evaluated. The inhibitory activity of WCC exposed to acidic conditions (pH 1.0 to 6.4) was stable, while heat-treated WCC (100℃, 10 min) showed slightly decreased inhibition activity. On combination assay with antibiotics frequently used in clinical practice, WCC was found to be an innocuous agent for antibiotic activity. These results suggest that daily intake of WCC is able to prevent H. pylori colonization in the stomach, and that it could be applied as adjuvant therapy in H. pylori eradication.Keywords: Helicobacter pylori, Chinese chive, Allium tuberosum, antibiotic resistance, growth inhibition effect, bactericidal activity * To whom correspondence should be addressed. *E-mail: htake@kochi-u.ac.jp (H. Takeuchi) tomokos@kochi-u.ac.jp (T. Shimamura) IntroductionHelicobacter pylori (H. pylori) was recognized as a human carcinogen by IARC in 1994(Sugiyama et al., 2002, and is a pathogenic gram-negative spiral microaerophilic bacterium that colonizes the human stomach in up to half the world's population (Rothenbacher and Brenner, 2003). H. pylori plays a major role in the development of gastro-duodenal diseases, including gastritis, peptic ulcer and gastric cancer, and is associated with a wide range of non-gastrointestinal tract conditions such as idiopathic thrombocytopenic purpura. As gastric cancer is one of the most frequent causes of cancer-related death, eradication of H. pylori can, therefore, contribute to the treatment and prevention of these diseases. Generally, H. pylori infection in clinical practice is treated with an effective regimen, a triple therapy consisting of a proton pump inhibitor and combinations of two antibiotics; amoxicillin (AMPC) and clarithromycin (CAM) or AMPC and metronidazole (MNZ) in Japan (Nishimori, et al., 2006). However, unsuccessful eradication therapy is increasing due to the increased occurrence of drug-resistant H. pylori (Nariman, et al., 2004). The appearance rates of drug-resistant H. pylori against AMPC, CAM and MNZ from 2007to 2009 were 0.4%, 19.4% and 25.7%, respectively (Lyudmila et al., 2010, and these rates are continuing to escalate.Instead of antibiotics, non-antibiotic substances derived from foods with anti-H. pylori activity are now a focus in Gastroenterology. There have been several reports on natural compounds derived from foods, includin...

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Identification of a d - glycero - d - manno -Heptosyltransferase Gene from Helicobacter pylori

Cited by 38 publications

References 60 publications

The redefinition of Helicobacter pylori lipopolysaccharide O-antigen and core-oligosaccharide domains

The redefinition of Helicobacter pylori lipopolysaccharide O-antigen and core-oligosaccharide domains

Microwave-assisted sample preparation for rapid and sensitive analysis of H. pylori lipid A applicable to a single colony

In Vitro Anti-Helicobacter pylori Activity of Chinese Chive (Allium tuberosum)

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