Insights from the redefinition of Helicobacter pylori lipopolysaccharide O-antigen and core-oligosaccharide domains
Authors:Hong Li1,2, Tiandi Yang3, Tingting Liao2, Aleksandra W. Debowski2,4, Hans-Olof Nilsson2, Stuart M. Haslam3, Anne Dell3, Keith A. Stubbs4, Barry J. Marshall2 and Mohammed Benghezal2,5
1 West China Marshall Research Center for Infectious Diseases, Center of Infectious Diseases, Division of Infectious Diseases, State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu 610041, China.
2 Helicobacter pylori Research Laboratory, School of Pathology & Laboratory Medicine, Marshall Centre for Infectious Disease Research and Training, University of Western Australia, Nedlands, Australia.
3 Department of Life Sciences, Imperial College London, South Kensington Campus, London, SW7 2AZ, United Kingdom.
4 School of Chemistry and Biochemistry, University of Western Australia, Crawley, Australia.
5 Swiss Vitamin Institute, Route de la Corniche 1, CH-1066 Epalinges, Switzerland.
Keywords:
Helicobacter pylori, lipopolysaccharide structure, persistence, therapy, antibiotic adjuvant.
Related Article(s)?
Li H, Yang T, Liao T, Debowski AW, Nilsson H-O, Fulurija A, Stuart M. Haslam, Barbara Mulloy, Anne Dell, Keith A. Stubbs, Barry J. Marshall, Mohammed Benghezal (2017). The redefinition of Helicobacter pylori lipopolysaccharide O-antigen and core-oligosaccharide domains. PLoS Pathog 13(3): e1006280. , 10.1371/journal.ppat.1006280
Corresponding Author(s):
Conflict of interest statement:
The funders had no role in the decision to publish this paper or its preparation. The authors disclose no conflicts of interests.
Please cite this article as:
Hong Li, Tiandi Yang, Tingting Liao, Aleksandra W. Debowski, Hans-Olof Nilsson, Stuart M. Has-lam, Anne Dell, Keith A. Stubbs, Barry J. Marshall and Mohammed Benghezal (2017). Insights from the redefinition of Helicobacter pylori lipopolysaccharide O-antigen and core-oligosaccharide domains. Microbial Cell 4(5):175-178. doi: 10.15698/mic2017.05.574
© 2017 Li et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.
Abstract:
H. pylori is a Gram-negative extracellular bacterium, first discovered by the Australian physicians Barry Marshall and Robin Warren in 1982, that colonises the human stomach mucosa. It is the leading cause of peptic ulcer and commonly infects humans worldwide with prevalence as high as 90% in some countries. H. pylori infection usually results in asymptomatic chronic gastritis, however 10-15% of cases develop duodenal or gastric ulcers and 1-3% develop stomach cancer. Infection is generally acquired during childhood and persists for life in the absence of antibiotic treatment. H. pylori has had a long period of co-evolution with humans, going back to human migration out of Africa. This prolonged relationship is likely to have shaped the overall host-pathogen interactions and repertoire of virulence strategies which H. pylori employs to establish robust colonisation, escape immune responses and persist in the gastric niche. In this regard, H. pylori lipopolysaccharide (LPS) is a key surface determinant in establishing colonisation and persistence via host mimicry and resistance to cationic antimicrobial peptides. Thus, elucidation of the H. pylori LPS structure and corresponding biosynthetic pathway represents an important step towards better understanding of H. pylori pathogenesis and the development of novel therapeutic interventions.
doi: 10.15698/mic2017.05.574
Volume 4, pp. 175 to 178, published 25/04/2017.