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Toxins
Special Issues
Helicobacter pylori Toxins and Pathogenesis
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Helicobacter pylori Toxins and Pathogenesis

A special issue of Toxins (ISSN 2072-6651). This special issue belongs to the section "Bacterial Toxins".

Deadline for manuscript submissions: closed (30 April 2021) | Viewed by 27163

Special Issue Editor

Prof. Dr. Yoshio Yamaoka

E-Mail Website
Guest Editor
Department of Environmental and Preventive Medicine, Oita University Faculty of Medicine, Idaigaoka, Hasama-machi, Yufu, Oita 879-5593, Japan
Interests: Helicobacter pylori; gastric cancer; virulence factors; epidemiology; human migration; antibiotics resistance; signal pathways; next generation sequencing
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Helicobacter pylori (Hp) is an important human pathogen that successfully colonizes the hostile stomach niche. This Gram-negative bacterium is mostly acquired during childhood before causing a lifelong infection that can generate pathologies ranging from chronic gastritis and peptic ulceration to gastric cancer. Several extragastric or extradigestive diseases have been also linked to Hp infection. Hp virulence factors causing direct cell damage that have been well characterized include the type IV secretion system (T4SS) encoded in the cag pathogenicity island (cag PAI) with its key multifunctional effector protein encoded by the cytotoxin-associated gene A (CagA), a vacuolating cytotoxin A (VacA), and an impressive set of ~60 outer membrane proteins (e.g., BabA, OipA, HopQ, AlpA, AlpB, etc.). Recently, the study of additional factors has gained momentum, including γ-glutamyl transpeptidase (GGT), high temperature requirement A (the serine protease HtrA), and cholesterol glycosyl-transferase (CGT). These Hp factors can be exposed at the bacterial surface, secreted as toxins in the immediate extracellular environment, or translocated into host cells as intracellular effectors. They can thus directly interact with host cellular pathways to hijack cellular functions in a pathogenic scheme or to evade assaults from immune systems. Our understanding of these bacterial factors and related signaling cascades has progressed substantially in recent years. However, several other questions are constantly arising in the field, calling for further study.  

The aim of this Special Issue is to provide an overview of the pathogenesis of Hp. Particular attention will be given to efforts directed toward depicting cellular pathways and finding putative new virulence factors or signaling cascades triggered by Hp. We welcome the submission of research articles, review articles, and short communications related to the various aspects of the pathogenesis of Hp: molecular epidemiology, cell signaling systems, virulence factors, and pathogen–host interaction or co-evolution. We believe that this Special Issue will give an updated insight into the exciting field of Hp and hope that provides new insights for future research activities.

As Guest Editor of this Special Issue, I look forward to reviewing your submissions and, together, defining the present state of the science.

Prof. Dr. Yoshio Yamaoka
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (6 papers)

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Research

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10 pages, 3170 KiB  
Article
Serodiagnosis and Bacterial Genome of Helicobacter pylori Infection
by Aina Ichihara, Hinako Ojima, Kazuyoshi Gotoh, Osamu Matsushita, Susumu Take, Hiroyuki Okada, Akari Watanabe and Kenji Yokota
Toxins 2021, 13(7), 467; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13070467 - 05 Jul 2021
Cited by 2 | Viewed by 2478
Abstract
The infection caused by Helicobacter pylori is associated with several diseases, including gastric cancer. Several methods for the diagnosis of H. pylori infection exist, including endoscopy, the urea breath test, and the fecal antigen test, which is the serum antibody titer test that [...] Read more.
The infection caused by Helicobacter pylori is associated with several diseases, including gastric cancer. Several methods for the diagnosis of H. pylori infection exist, including endoscopy, the urea breath test, and the fecal antigen test, which is the serum antibody titer test that is often used since it is a simple and highly sensitive test. In this context, this study aims to find the association between different antibody reactivities and the organization of bacterial genomes. Next-generation sequences were performed to determine the genome sequences of four strains of antigens with different reactivity. The search was performed on the common genes, with the homology analysis conducted using a genome ring and dot plot analysis. The two antigens of the highly reactive strains showed a high gene homology, and Western blots for CagA and VacA also showed high expression levels of proteins. In the poorly responsive antigen strains, it was found that the inversion occurred around the vacA gene in the genome. The structure of bacterial genomes might contribute to the poor reactivity exhibited by the antibodies of patients. In the future, an accurate serodiagnosis could be performed by using a strain with few gene mutations of the antigen used for the antibody titer test of H. pylori. Full article
(This article belongs to the Special Issue Helicobacter pylori Toxins and Pathogenesis)
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20 pages, 4264 KiB  
Article
Whole Genome Sequencing Reveals Virulence Potentials of Helicobacter pylori Strain KE21 Isolated from a Kenyan Patient with Gastric Signet Ring Cell Carcinoma
by Catherine Mwangi, Stephen Njoroge, Evariste Tshibangu-Kabamba, Zahir Moloo, Allan Rajula, Smita Devani, Takashi Matsumoto, Kimang’a Nyerere, Samuel Kariuki, Gunturu Revathi and Yoshio Yamaoka
Toxins 2020, 12(9), 556; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins12090556 - 29 Aug 2020
Cited by 11 | Viewed by 5441
Abstract
Helicobacter pylori (H.pylori) infection is etiologically associated with severe diseases including gastric cancer; but its pathogenicity is deeply shaped by the exceptional genomic diversification and geographic variation of the species. The clinical relevance of strains colonizing Africa is still debated. This [...] Read more.
Helicobacter pylori (H.pylori) infection is etiologically associated with severe diseases including gastric cancer; but its pathogenicity is deeply shaped by the exceptional genomic diversification and geographic variation of the species. The clinical relevance of strains colonizing Africa is still debated. This study aimed to explore genomic features and virulence potentials of H. pylori KE21, a typical African strain isolated from a native Kenyan patient diagnosed with a gastric cancer. A high-quality circular genome assembly of 1,648,327 bp (1590 genes) obtained as a hybrid of Illumina Miseq short reads and Oxford Nanopore MinION long reads, clustered within hpAfrica1 population. This genome revealed a virulome and a mobilome encoding more than hundred features potentiating a successful colonization, persistent infection, and enhanced disease pathogenesis. Furthermore, through an experimental infection of gastric epithelial cell lines, strain KE21 showed the ability to promote interleukin-8 production and to induce cellular alterations resulting from the injection of a functional CagA oncogene protein into the cells. This study shows that strain KE21 is potentially virulent and can trigger oncogenic pathways in gastric epithelial cells. Expended genomic and clinical explorations are required to evaluate the epidemiological importance of H. pylori infection and its putative complications in the study population. Full article
(This article belongs to the Special Issue Helicobacter pylori Toxins and Pathogenesis)
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14 pages, 1788 KiB  
Article
Biofilm Formation and Antibiotic Resistance Phenotype of Helicobacter pylori Clinical Isolates
by Kartika Afrida Fauzia, Muhammad Miftahussurur, Ari Fahrial Syam, Langgeng Agung Waskito, Dalla Doohan, Yudith Annisa Ayu Rezkitha, Takashi Matsumoto, Vo Phuoc Tuan, Junko Akada, Hideo Yonezawa, Shigeru Kamiya and Yoshio Yamaoka
Toxins 2020, 12(8), 473; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins12080473 - 24 Jul 2020
Cited by 28 | Viewed by 4829
Abstract
We evaluated biofilm formation of clinical Helicobacter pylori isolates from Indonesia and its relation to antibiotic resistance. We determined the minimum inhibition concentration (MIC) of amoxicillin, clarithromycin, levofloxacin, metronidazole and tetracycline by the Etest to measure the planktonic susceptibility of 101 H. pylori [...] Read more.
We evaluated biofilm formation of clinical Helicobacter pylori isolates from Indonesia and its relation to antibiotic resistance. We determined the minimum inhibition concentration (MIC) of amoxicillin, clarithromycin, levofloxacin, metronidazole and tetracycline by the Etest to measure the planktonic susceptibility of 101 H. pylori strains. Biofilms were quantified by the crystal violet method. The minimum biofilm eradication concentration (MBEC) was obtained by measuring the survival of bacteria in a biofilm after exposure to antibiotics. The majority of the strains formed a biofilm (93.1% (94/101)), including weak (75.5%) and strong (24.5%) biofilm-formers. Planktonic resistant and sensitive strains produced relatively equal amounts of biofilms. The resistance proportion, shown by the MBEC measurement, was higher in the strong biofilm group for all antibiotics compared to the weak biofilm group, especially for clarithromycin (p = 0.002). Several cases showed sensitivity by the MIC measurement, but resistance according to the MBEC measurements (amoxicillin, 47.6%; tetracycline, 57.1%; clarithromycin, 19.0%; levofloxacin, 38.1%; and metronidazole 38.1%). Thus, biofilm formation may increase the survival of H. pylori and its resistance to antibiotics. Biofilm-related antibiotic resistance should be evaluated with antibiotic susceptibility. Full article
(This article belongs to the Special Issue Helicobacter pylori Toxins and Pathogenesis)
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Review

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12 pages, 521 KiB  
Review
Helicobacter pylori BabA–SabA Key Roles in the Adherence Phase: The Synergic Mechanism for Successful Colonization and Disease Development
by Dalla Doohan, Yudith Annisa Ayu Rezkitha, Langgeng Agung Waskito, Yoshio Yamaoka and Muhammad Miftahussurur
Toxins 2021, 13(7), 485; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13070485 - 13 Jul 2021
Cited by 36 | Viewed by 5720
Abstract
Helicobacter pylori is a pathogenic microorganism that successfully inhabits the human stomach, colonizing it by producing several virulence factors responsible for preventing host self-defense mechanisms. The adherence mechanism to gastric mucosal tissue is one of the most important processes for effective colonization in [...] Read more.
Helicobacter pylori is a pathogenic microorganism that successfully inhabits the human stomach, colonizing it by producing several virulence factors responsible for preventing host self-defense mechanisms. The adherence mechanism to gastric mucosal tissue is one of the most important processes for effective colonization in the stomach. The blood group antigen-binding adhesion (BabA) and sialic acid-binding adherence (SabA) are two H. pylori outer membrane proteins able to interact with antigens in the gastroduodenal tract. H. pylori possesses several mechanisms to control the regulation of both BabA and SabA in either the transcriptional or translational level. BabA is believed to be the most important protein in the early infection phase due to its ability to interact with various Lewis antigens, whereas SabA interaction with sialylated Lewis antigens may prove important for the adherence process in the inflamed gastric mucosal tissue in the ongoing-infection phase. The adherence mechanisms of BabA and SabA allow H. pylori to anchor in the gastric mucosa and begin the colonization process. Full article
(This article belongs to the Special Issue Helicobacter pylori Toxins and Pathogenesis)
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19 pages, 1423 KiB  
Review
The Roles of IL-17, IL-21, and IL-23 in the Helicobacter pylori Infection and Gastrointestinal Inflammation: A Review
by Astri Dewayani, Kartika Afrida Fauzia, Ricky Indra Alfaray, Langgeng Agung Waskito, Dalla Doohan, Yudith Annisa Ayu Rezkitha, Abdurachman Abdurachman, Takashi Kobayashi, Reny I’tishom, Yoshio Yamaoka and Muhammad Miftahussurur
Toxins 2021, 13(5), 315; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13050315 - 28 Apr 2021
Cited by 21 | Viewed by 4129
Abstract
Although millions of people have been infected by Helicobacter pylori (H. pylori), only a small proportion of infected individuals will develop adverse outcomes, ranging from chronic gastritis to gastric cancer. Advanced development of the disease has been well-linked with chronic inflammation, [...] Read more.
Although millions of people have been infected by Helicobacter pylori (H. pylori), only a small proportion of infected individuals will develop adverse outcomes, ranging from chronic gastritis to gastric cancer. Advanced development of the disease has been well-linked with chronic inflammation, which is significantly impacted by the adaptive and humoral immunity response. From the perspective of cellular immunity, this review aims to clarify the intricate axis between IL-17, IL-21, and IL-23 in H. pylori-related diseases and the pathogenesis of inflammatory gastrointestinal diseases. CD4+ helper T (Th)-17 cells, with the hallmark pleiotropic cytokine IL-17, can affect antimicrobial activity and the pathogenic immune response in the gut environment. These circumstances cannot be separated, as the existence of affiliated cytokines, including IL-21 and IL-23, help maintain Th17 and accommodate humoral immune cells. Comprehensive understanding of the dynamic interaction between molecular host responses in H. pylori-related diseases and the inflammation process may facilitate further development of immune-based therapy. Full article
(This article belongs to the Special Issue Helicobacter pylori Toxins and Pathogenesis)
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13 pages, 12055 KiB  
Review
Role of TNF-α-Inducing Protein Secreted by Helicobacter pylori as a Tumor Promoter in Gastric Cancer and Emerging Preventive Strategies
by Masami Suganuma, Tatsuro Watanabe, Eisaburo Sueoka, In Kyoung Lim and Hirota Fujiki
Toxins 2021, 13(3), 181; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13030181 - 01 Mar 2021
Cited by 14 | Viewed by 3458
Abstract
The tumor necrosis factor-α (TNF-α)-inducing protein (tipα) gene family, comprising Helicobacter pylori membrane protein 1 (hp-mp1) and tipα, has been identified as a tumor promoter, contributing to H. pylori carcinogenicity. Tipα is a unique H. pylori protein with no similarity to other [...] Read more.
The tumor necrosis factor-α (TNF-α)-inducing protein (tipα) gene family, comprising Helicobacter pylori membrane protein 1 (hp-mp1) and tipα, has been identified as a tumor promoter, contributing to H. pylori carcinogenicity. Tipα is a unique H. pylori protein with no similarity to other pathogenicity factors, CagA, VacA, and urease. American H. pylori strains cause human gastric cancer, whereas African strains cause gastritis. The presence of Tipα in American and Euro-Asian strains suggests its involvement in human gastric cancer development. Tipα secreted from H. pylori stimulates gastric cancer development by inducing TNF-α, an endogenous tumor promoter, through its interaction with nucleolin, a Tipα receptor. This review covers the following topics: tumor-promoting activity of the Tipα family members HP-MP1 and Tipα, the mechanism underlying this activity of Tipα via binding to the cell-surface receptor, nucleolin, the crystal structure of rdel-Tipα and N-terminal truncated rTipα, inhibition of Tipα-associated gastric carcinogenesis by tumor suppressor B-cell translocation gene 2 (BTG2/TIS21), and new strategies to prevent and treat gastric cancer. Thus, Tipα contributes to the carcinogenicity of H. pylori by a mechanism that differs from those of CagA and VacA. Full article
(This article belongs to the Special Issue Helicobacter pylori Toxins and Pathogenesis)
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