41
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Helicobacter pylori Virulence Factors Exploiting Gastric Colonization and its Pathogenicity

      review-article
      1 , 2 , 3 , 4 , 5 , *
      Toxins
      MDPI
      Helicobacter pylori, gastritis, peptic ulcer, gastric cancer, CagA, cagPAI

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Helicobacter pylori colonizes the gastric epithelial cells of at least half of the world’s population, and it is the strongest risk factor for developing gastric complications like chronic gastritis, ulcer diseases, and gastric cancer. To successfully colonize and establish a persistent infection, the bacteria must overcome harsh gastric conditions. H. pylori has a well-developed mechanism by which it can survive in a very acidic niche. Despite bacterial factors, gastric environmental factors and host genetic constituents together play a co-operative role for gastric pathogenicity. The virulence factors include bacterial colonization factors BabA, SabA, OipA, and HopQ, and the virulence factors necessary for gastric pathogenicity include the effector proteins like CagA, VacA, HtrA, and the outer membrane vesicles. Bacterial factors are considered more important. Here, we summarize the recent information to better understand several bacterial virulence factors and their role in the pathogenic mechanism.

          Related collections

          Most cited references205

          • Record: found
          • Abstract: found
          • Article: not found

          Pathobiology of Helicobacter pylori-Induced Gastric Cancer.

          Colonization of the human stomach by Helicobacter pylori and its role in causing gastric cancer is one of the richest examples of a complex relationship among human cells, microbes, and their environment. It is also a puzzle of enormous medical importance given the incidence and lethality of gastric cancer worldwide. We review recent findings that have changed how we view these relationships and affected the direction of gastric cancer research. For example, recent data have indicated that subtle mismatches between host and microbe genetic traits greatly affect the risk of gastric cancer. The ability of H pylori and its oncoprotein CagA to reprogram epithelial cells and activate properties of stemness show the sophisticated relationship between H pylori and progenitor cells in the gastric mucosa. The observation that cell-associated H pylori can colonize the gastric glands and directly affect precursor and stem cells supports these observations. The ability to mimic these interactions in human gastric organoid cultures as well as animal models will allow investigators to more fully unravel the extent of H pylori control on the renewing gastric epithelium. Finally, our realization that external environmental factors, such as dietary components and essential micronutrients, as well as the gastrointestinal microbiota, can change the balance between H pylori's activity as a commensal or a pathogen has provided direction to studies aimed at defining the full carcinogenic potential of this organism.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: found
            Is Open Access

            Gastric microbial community profiling reveals a dysbiotic cancer-associated microbiota

            Objective Gastric carcinoma development is triggered by Helicobacter pylori. Chronic H. pylori infection leads to reduced acid secretion, which may allow the growth of a different gastric bacterial community. This change in the microbiome may increase aggression to the gastric mucosa and contribute to malignancy. Our aim was to evaluate the composition of the gastric microbiota in chronic gastritis and in gastric carcinoma. Design The gastric microbiota was retrospectively investigated in 54 patients with gastric carcinoma and 81 patients with chronic gastritis by 16S rRNA gene profiling, using next-generation sequencing. Differences in microbial composition of the two patient groups were assessed using linear discriminant analysis effect size. Associations between the most relevant taxa and clinical diagnosis were validated by real-time quantitative PCR. Predictive functional profiling of microbial communities was obtained with PICRUSt. Results The gastric carcinoma microbiota was characterised by reduced microbial diversity, by decreased abundance of Helicobacter and by the enrichment of other bacterial genera, mostly represented by intestinal commensals. The combination of these taxa into a microbial dysbiosis index revealed that dysbiosis has excellent capacity to discriminate between gastritis and gastric carcinoma. Analysis of the functional features of the microbiota was compatible with the presence of a nitrosating microbial community in carcinoma. The major observations were confirmed in validation cohorts from different geographic origins. Conclusions Detailed analysis of the gastric microbiota revealed for the first time that patients with gastric carcinoma exhibit a dysbiotic microbial community with genotoxic potential, which is distinct from that of patients with chronic gastritis.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Nod1 responds to peptidoglycan delivered by the Helicobacter pylori cag pathogenicity island.

              Epithelial cells can respond to conserved bacterial products that are internalized after either bacterial invasion or liposome treatment of cells. We report here that the noninvasive Gram-negative pathogen Helicobacter pylori was recognized by epithelial cells via Nod1, an intracellular pathogen-recognition molecule with specificity for Gram-negative peptidoglycan. Nod1 detection of H. pylori depended on the delivery of peptidoglycan to host cells by a bacterial type IV secretion system, encoded by the H. pylori cag pathogenicity island. Consistent with involvement of Nod1 in host defense, Nod1-deficient mice were more susceptible to infection by cag pathogenicity island-positive H. pylori than were wild-type mice. We propose that sensing of H. pylori by Nod1 represents a model for host recognition of noninvasive pathogens.
                Bookmark

                Author and article information

                Journal
                Toxins (Basel)
                Toxins (Basel)
                toxins
                Toxins
                MDPI
                2072-6651
                19 November 2019
                November 2019
                : 11
                : 11
                : 677
                Affiliations
                [1 ]Department of Microbiology, Chitwan Medical College and Teaching Hospital, Bharatpur 44200, Chitwan, Nepal; shamshulansari483@ 123456yahoo.com
                [2 ]Department of Environmental and Preventive Medicine, Oita University Faculty of Medicine, Idaigaoka, Hasama-machi, Yufu, Oita 879-5593, Japan
                [3 ]Global Oita Medical Advanced Research Center for Health, Idaigaoka, Hasama-machi, Yufu, Oita 879-5593, Japan
                [4 ]Department of Medicine, Gastroenterology and Hepatology Section, Baylor College of Medicine, 2002 Holcombe Blvd., Houston, TX 77030, USA
                [5 ]Borneo Medical and Health Research Centre, Universiti Malaysia Sabah, Kota Kinabaru, Sabah 88400, Malaysia
                Author notes
                [* ]Correspondence: yyamaoka@ 123456oita-u.ac.jp
                Author information
                https://orcid.org/0000-0003-1846-1377
                https://orcid.org/0000-0002-1222-5819
                Article
                toxins-11-00677
                10.3390/toxins11110677
                6891454
                31752394
                e805abcc-2362-4ccc-8e97-3bee159d586a
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 23 October 2019
                : 16 November 2019
                Categories
                Review

                Molecular medicine
                helicobacter pylori,gastritis,peptic ulcer,gastric cancer,caga,cagpai
                Molecular medicine
                helicobacter pylori, gastritis, peptic ulcer, gastric cancer, caga, cagpai

                Comments

                Comment on this article