Frequency of endoscopic findings of equine squamous gastric disease (ESGD) in rural horses and its association with Helicobacter pylori virulence genes

Equine gastric ulcer syndrome (EGUS) is a multifactorial disorder and one of the most common diseases in horses. The objective of this research was to detect one of the potential risk factors of equine squamous gastric disease (ESGD), the Helicobacter pylori specific gene, and tracing the presence of the duodenal ulcer-promoting gene (dupA) as a possible virulence marker. Gastric fluid together with faecal samples were collected from twenty rural horses from around Tabriz, Iran. Throughout the endoscopic examinations, the type, numbers, severity, and the location of the lesions were documented. Nine of twenty horses exhibited macroscopic lesions in the squamous mucosa that were later classified into grades 1, 2, 3, and 4. Only three of these horses exhibited H. pylori in their gastric fluid samples, whereas all faecal samples were H. pylori-negative. All the H. pylori-positive cases manifested severe forms of ESGD (grades 3–4). The age and sex were both unrelated to the lesion severity and ESGD status in this study. Research is required to further discuss the virulence aspects of dupA regarding ESGD.

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Intracellular Presence of Helicobacter pylori and Its Virulence-Associated Genotypes within the Vaginal Yeast of Term Pregnant Women

Microorganisms ◽

10.3390/microorganisms9010131 ◽

2021 ◽

Vol 9 (1) ◽

pp. 131

Author(s):

Kimberly Sánchez-Alonzo ◽

Lillian Matamala-Valdés ◽

Cristian Parra-Sepúlveda ◽

Humberto Bernasconi ◽

Víctor L. Campos ◽

...

Keyword(s):

Risk Factors ◽

Helicobacter Pylori ◽

Virulence Genes ◽

Yeast Cells ◽

Bacterial Identification ◽

Infection Risk Factors ◽

Horse Blood ◽

Total Dna ◽

H Pylori ◽

Total Yeast

Background: Helicobacter pylori transmission routes are not entirely elucidated. Since yeasts are postulated to transmit this pathogen, this study aimed to detect and genotype intracellular H. pylori harbored within vaginal yeast cells. Methods: A questionnaire was used to determine risk factors of H. pylori infection. Samples were seeded on Sabouraud Dextrose Agar and horse blood-supplemented Columbia agar. Isolated yeasts were identified using and observed by optical microscopy searching for intra-yeast H. pylori. Total yeast DNA, from one random sample, was extracted to search for H. pylori virulence genes by PCR and bacterial identification by sequencing. Results: 43% of samples contained yeasts, mainly Candida albicans (91%). Microscopy detected bacteria such as bodies and anti-H. pylori antibodies binding particles in 50% of the isolated yeasts. Total DNA extracted showed that 50% of the isolated yeasts were positive for H. pylori 16S rDNA and the sequence showed 99.8% similarity with H. pylori. In total, 32% of H. pylori DNA positive samples were cagA+ vacAs1a vacAm1 dupA−. No relationship was observed between possible H. pylori infection risk factors and vaginal yeasts harboring this bacterium. Conclusion: H. pylori having virulent genotypes were detected within vaginal yeasts constituting a risk for vertical transmission of this pathogen.

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Prevalence of vacA, cagA, and iceA Virulence Factors of Helicobacter Pylori Isolated from Gastro-duodenal Patients

Journal of Biotechnology Research Center ◽

10.24126/jobrc.2020.14.1.592 ◽

2020 ◽

Vol 14 (1) ◽

pp. 72-79

Author(s):

Ahmed Husham Salman ◽

Aumed Arshad Hawezy

Keyword(s):

Helicobacter Pylori ◽

Virulence Factors ◽

Virulence Genes ◽

Gastric Lymphoma ◽

Signs And Symptoms ◽

Molecular Technique ◽

Peptic Ulcers ◽

Back Ground ◽

H Pylori ◽

Pcr Test

Back ground: Helicobacter pylori are bacteria colonize in the human epithelial cells of the gastrointestinal tract. Its infection causes different diseases, including chronic gastritis, peptic ulcers, gastric lymphoma and adenocarcinoma. H. pylori have many virulence factors attributing in one or more biological functions. Objective: Detecting the prevalence of virulence factor genes vacA, cagA, iceA among strain of H. pylori using molecular technique (PCR). Materials and methods: Sixty patients (27 male and 33 female), aged 18 and above included in the present study who showed signs and symptoms of H. pylori, and undergo endoscopy between period of November 2019 and February 2020. RUT and PCR test done to detect the presence of H. pylori infection, also PCR used to detect the three virulence factors. Results: Result showed that 44 patients, 21 (47.7%) male and 23 (52.3%) female were detected as positive H. pylori infections, among them 13 (29.5%) above 50 years, and 31 (70.4%) were below 50 years. While prevalence of the virulence factors vacA, cagA, and iceA were (100%), (84.1%), and (34.1%) respectively. Conclusion: It can be concluded that the frequency and prevalence of these genes are differed and showed significant differences among them. Also, PCR test is sensitive and accurate for detection of H. pylori virulence genes.

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Role of Interleukin-32 in Helicobacter pylori-Induced Gastric Inflammation

Infection and Immunity ◽

10.1128/iai.00637-12 ◽

2012 ◽

Vol 80 (11) ◽

pp. 3795-3803 ◽

Cited By ~ 31

Author(s):

Kosuke Sakitani ◽

Yoshihiro Hirata ◽

Yoku Hayakawa ◽

Takako Serizawa ◽

Wachiko Nakata ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Gastric Mucosa ◽

Cell Lines ◽

Inflammatory Diseases ◽

Nuclear Factor Κb ◽

Gastric Disease ◽

Ags Cells ◽

Content Type ◽

H Pylori

ABSTRACTHelicobacter pyloriinfection is associated with gastritis and gastric cancer. AnH. pylorivirulence factor, thecagpathogenicity island (PAI), is related to host cell cytokine induction and gastric inflammation. Since elucidation of the mechanisms of inflammation is important for therapy, the associations between cytokines and inflammatory diseases have been investigated vigorously. Levels of interleukin-32 (IL-32), a recently described inflammatory cytokine, are increased in various inflammatory diseases, such as rheumatoid arthritis and Crohn's disease, and in malignancies, including gastric cancer. In this report, we examined IL-32 expression in human gastric disease. We also investigated the function of IL-32 in activation of the inflammatory cytokines in gastritis. IL-32 expression paralleled human gastric tissue pathology, with low IL-32 expression inH. pylori-uninfected gastric mucosa and higher expression levels in gastritis and gastric cancer tissues.H. pyloriinfection increased IL-32 expression in human gastric epithelial cell lines.H. pylori-induced IL-32 expression was dependent on the bacterialcagPAI genes and on activation of nuclear factor κB (NF-κB). IL-32 expression induced byH. pyloriwas not detected in the supernatant of AGS cells but was found in the cytosol. Expression of theH. pylori-induced cytokines CXCL1, CXCL2, and IL-8 was decreased in IL-32-knockdown AGS cell lines compared to a control AGS cell line. We also found that NF-κB activation was decreased inH. pylori-infected IL-32-knockdown cells. These results suggest that IL-32 has important functions in the regulation of cytokine expression inH. pylori-infected gastric mucosa.

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Phylogeographic Origin of Helicobacter pylori Determines Host-Adaptive Responses upon Coculture with Gastric Epithelial Cells

Infection and Immunity ◽

10.1128/iai.01182-12 ◽

2013 ◽

Vol 81 (7) ◽

pp. 2468-2477 ◽

Cited By ~ 16

Author(s):

Alexander Sheh ◽

Rupesh Chaturvedi ◽

D. Scott Merrell ◽

Pelayo Correa ◽

Keith T. Wilson ◽

...

Keyword(s):

Gene Expression ◽

Gastric Cancer ◽

Helicobacter Pylori ◽

Epithelial Cells ◽

Gastric Disease ◽

Gastric Epithelial Cells ◽

Gastric Cancer Risk ◽

Content Type ◽

H Pylori ◽

Induced Apoptosis

ABSTRACTWhileHelicobacter pyloriinfects over 50% of the world's population, the mechanisms involved in the development of gastric disease are not fully understood. Bacterial, host, and environmental factors play a role in disease outcome. To investigate the role of bacterial factors inH. pyloripathogenesis, global gene expression of sixH. pyloriisolates was analyzed during coculture with gastric epithelial cells. Clustering analysis of six Colombian clinical isolates from a region with low gastric cancer risk and a region with high gastric cancer risk segregated strains based on their phylogeographic origin. One hundred forty-six genes had increased expression in European strains, while 350 genes had increased expression in African strains. Differential expression was observed in genes associated with motility, pathogenicity, and other adaptations to the host environment. European strains had greater expression of the virulence factorscagA,vacA, andbabBand were associated with increased gastric histologic lesions in patients. In AGS cells, European strains promoted significantly higher interleukin-8 (IL-8) expression than did African strains. African strains significantly induced apoptosis, whereas only one European strain significantly induced apoptosis. Our data suggest that gene expression profiles of clinical isolates can discriminate strains by phylogeographic origin and that these profiles are associated with changes in expression of the proinflammatory and protumorigenic cytokine IL-8 and levels of apoptosis in host epithelial cells. These findings support the hypothesis that bacterial factors determined by the phylogeographic origin ofH. pyloristrains may promote increased gastric disease.

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Eradication of Helicobacter pylori and Gastric Cancer: A Controversial Relationship

Frontiers in Microbiology ◽

10.3389/fmicb.2021.630852 ◽

2021 ◽

Vol 12 ◽

Author(s):

Mariagrazia Piscione ◽

Mariangela Mazzone ◽

Maria Carmela Di Marcantonio ◽

Raffaella Muraro ◽

Gabriella Mincione

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Atrophic Gastritis ◽

Precancerous Lesions ◽

Eradication Therapy ◽

Developed Countries ◽

Gastric Carcinogenesis ◽

Gastric Disease ◽

Type I ◽

H Pylori

Worldwide, gastric cancer (GC) represents the fifth cancer for incidence, and the third as cause of death in developed countries. Indeed, it resulted in more than 780,000 deaths in 2018. Helicobacter pylori appears to be responsible for the majority of these cancers. On the basis of recent studies, and either alone or combined with additional etiological factors, H. pylori is considered a “type I carcinogen.” Over recent decades, new insights have been obtained into the strategies that have been adopted by H. pylori to survive the acidic conditions of the gastric environment, and to result in persistent infection, and dysregulation of host functions. The multistep processes involved in the development of GC are initiated by transition of the mucosa into chronic non-atrophic gastritis, which is primarily triggered by infection with H. pylori. This gastritis then progresses into atrophic gastritis and intestinal metaplasia, and then to dysplasia, and following Correa’s cascade, to adenocarcinoma. The use of antibiotics for eradication of H. pylori can reduce the incidence of precancerous lesions only in the early stages of gastric carcinogenesis. Here, we first survey the etiology and risk factors of GC, and then we analyze the mechanisms underlying tumorigenesis induced by H. pylori, focusing attention on virulence factor CagA, inflammation, oxidative stress, and ErbB2 receptor tyrosine kinase. Moreover, we investigate the relationships between H. pylori eradication therapy and other diseases, considering not only cardia (upper stomach) cancers and Barrett’s esophagus, but also asthma and allergies, through discussion of the “hygiene hypothesis. ” This hypothesis suggests that improved hygiene and antibiotic use in early life reduces microbial exposure, such that the immune response does not become primed, and individuals are not protected against atopic disorders, asthma, and autoimmune diseases. Finally, we overview recent advances to uncover the complex interplay between H. pylori and the gut microbiota during gastric carcinogenesis, as characterized by reduced bacterial diversity and increased microbial dysbiosis. Indeed, it is of particular importance to identify the bacterial taxa of the stomach that might predict the outcome of gastric disease through the stages of Correa’s cascade, to improve prevention and therapy of gastric carcinoma.

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Tailor-Made Detection of Individual Phosphorylated and Non-Phosphorylated EPIYA-Motifs of Helicobacter pylori Oncoprotein CagA

Cancers ◽

10.3390/cancers11081163 ◽

2019 ◽

Vol 11 (8) ◽

pp. 1163 ◽

Cited By ~ 1

Author(s):

Pachathundikandi ◽

Gutiérrez-Escobar ◽

Tegtmeyer

Keyword(s):

Helicobacter Pylori ◽

Cross Reactivity ◽

Host Cells ◽

Gastric Disease ◽

Effector Protein ◽

Sequence Motifs ◽

Type Iv ◽

Efficient Detection ◽

H Pylori ◽

Epiya Motifs

The gastric pathogen and carcinogen Helicobacter pylori (H. pylori) encodes a type IV secretion system for translocation of the effector protein CagA into host cells. Injected CagA becomes tyrosine-phosphorylated at the five amino acid residue Glutamate-Proline- Isoleucine-Tyrosine-Alanine (EPIYA)-sequence motifs. These phosphorylated EPIYA-sites represent recognition motifs for binding of multiple host factors, which then manipulate signaling pathways to trigger gastric disease. Thus, efficient detection of single phosphorylated EPIYA-motifs in CagA is required. Detection of phospho-CagA is primarily performed using commercial pan-phosphotyrosine antibodies. However, those antibodies were originally generated to recognize many phosphotyrosines in various mammalian proteins and are not optimized for use in bacteria. To address this important limitation, we synthesized 11-mer phospho- and non-phospho-peptides from EPIYA-motifs A, B, and C, and produced three phospho-specific and three non-phospho-specific rabbit polyclonal CagA antibodies. These antibodies specifically recognized the corresponding phosphorylated and non-phosphorylated EPIYA-motifs, while the EPIYA-C antibodies also recognized the related East-Asian EPIYA-D motif. Otherwise, no cross-reactivity of the antibodies among EPIYAs was observed. Western blotting demonstrated that each EPIYA-motif can be predominantly phosphorylated during H. pylori infection. This represents the first complete set of phospho-specific antibodies for an effector protein in bacteria, providing useful tools to gather information for the categorization of CagA phosphorylation, cancer signaling, and gastric disease progression.

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Gene structure of the Helicobacter pylori cytotoxin and evidence of its key role in gastric disease.

Journal of Experimental Medicine ◽

10.1084/jem.179.5.1653 ◽

1994 ◽

Vol 179 (5) ◽

pp. 1653-1658 ◽

Cited By ~ 383

Author(s):

J L Telford ◽

P Ghiara ◽

M Dell'Orco ◽

M Comanducci ◽

D Burroni ◽

...

Keyword(s):

Helicobacter Pylori ◽

Peptic Ulcer ◽

Gastric Mucosa ◽

Chronic Infection ◽

Gastric Disease ◽

Human Gastric Mucosa ◽

Gastric Lesions ◽

Gram Negative ◽

H Pylori ◽

Cytotoxin Gene

The gram negative, microaerophilic bacterium Helicobacter pylori colonizes the human gastric mucosa and establishes a chronic infection that is tightly associated with atrophic gastritis, peptic ulcer, and gastric carcinoma. Cloning of the H. pylori cytotoxin gene shows that the protein is synthesized as a 140-kD precursor that is processed to a 94-kD fully active toxin. Oral administration to mice of the purified 94-kD protein caused ulceration and gastric lesions that bear some similarities to the pathology observed in humans. The cloning of the cytotoxin gene and the development of a mouse model of human gastric disease will provide the basis for the understanding of H. pylori pathogenesis and the development of therapeutics and vaccines.

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Host Epithelial Interactions with Helicobacter Pylori: A Role for Disrupted Gastric Barrier Function in the Clinical Outcome of Infection?

Canadian Journal of Gastroenterology ◽

10.1155/2005/940213 ◽

2005 ◽

Vol 19 (9) ◽

pp. 543-552 ◽

Cited By ~ 3

Author(s):

Andre G Buret ◽

Jason P Fedwick ◽

Andrew N Flynn

Keyword(s):

Helicobacter Pylori ◽

Clinical Outcome ◽

Barrier Function ◽

Gastric Disease ◽

Gastrointestinal Infections ◽

Epithelial Barrier Function ◽

Control Disease ◽

H Pylori ◽

Gastric Permeability ◽

Gastric Barrier

Infection of the human stomach with Helicobacter pylori may develop into gastritis, ulceration, adenocarcinoma and mucosal lymphomas. The pathogenic mechanisms that determine the clinical outcome from this microbial-epithelial interaction remain poorly understood. An increasing number of reports suggests that disruptions of epithelial barrier function may contribute to pathology and postinfectious complications in a variety of gastrointestinal infections. The aim of this review is to critically discuss the implications of H pylori persistence on gastric disease, with emphasis on the role of myosin light chain kinase, claudins and matrix metalloproteinases in gastric permeability defects, and their contribution to the development of cancer. These mechanisms and the associated signalling events may represent novel therapeutic targets to control disease processes induced by H pylori, a microbial pathogen that colonizes the stomach of over 50% of the human population.

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OralHelicobacter pylori: Can We Stomach It?

Critical Reviews in Oral Biology & Medicine ◽

10.1177/154411130301400307 ◽

2003 ◽

Vol 14 (3) ◽

pp. 226-233 ◽

Cited By ~ 61

Author(s):

S.A. Dowsett ◽

M.J. Kowolik

Keyword(s):

Helicobacter Pylori ◽

Oral Cavity ◽

Dental Plaque ◽

Human Stomach ◽

Future Research ◽

Gastric Disease ◽

Transmission Process ◽

Dental Profession ◽

H Pylori

Helicobacter pylori infection is one of the most common in man. The bacterium primarily resides in the human stomach, where it plays a significant role in gastric disease. If the spread of H. pylori is to be prevented, an understanding of the transmission process is essential. The oral cavity has been proposed as a reservoir for gastric H. pylori, which has been detected by culture and PCR in both dental plaque and saliva. This review will discuss the evidence for the role of the oral cavity in the transmission of gastric H. pylori. Moreover, the difficulties encountered in addressing this topic, possible directions for future research, and the implications for the dental profession are discussed.

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Precancerous Gastric Lesions with Helicobacter pylori vacA+/babA2+/oipA+ Genotype Increase the Risk of Gastric Cancer

BioMed Research International ◽

10.1155/2020/7243029 ◽

2020 ◽

Vol 2020 ◽

pp. 1-8 ◽

Cited By ~ 1

Author(s):

Theeraya Simawaranon Bartpho ◽

Wareeporn Wattanawongdon ◽

Taweesak Tongtawee ◽

Chatchanok Paoin ◽

Kokiet Kangwantas ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Clinical Outcomes ◽

Chronic Gastritis ◽

Virulence Genes ◽

Gastric Lesions ◽

Precancerous Gastric Lesions ◽

Increased Risk ◽

H Pylori ◽

Gastric Cancer Patients

Objective. The clinical outcomes of gastric diseases such as chronic gastritis, peptic ulcer, and gastric cancer have been attributed to the interplay of virulence factors of Helicobacter pylori (H. pylori), host genetic susceptibility, and host immune responses. This study investigated the presence of cagA, vacA, iceA2, babA2, and oipA genes and their association with clinical outcomes. Methods. Chronic gastritis, atrophic gastritis, and intestinal metaplasia specimens were obtained from patients who underwent endoscopy and surgical resection between January 2017 and December 2018; specimens from gastric cancer patients treated between January 2014 and December 2018 were also added. H. pylori infection and virulence genes (cagA, vacA, iceA2, babA2, and oipA) were determined using real-time PCR. The association between H. pylori genotypes and clinical outcomes were evaluated using multivariate regression model analysis. The overall survival of gastric cancer patients was compared between genotype combinations. Results. H. pylori was positive in 166 patients with chronic gastritis, precancerous gastric lesions, and gastric cancer. The genes vacA, babA2, and oipA were most prevalent in chronic gastritis (73%), precancerous gastric lesions (62%), and gastric cancer (91%), respectively. The vacA, babA2, and oipA genes were associated with increased risk of gastric cancer (OR = 1.23; 95% CI = 1.13–3.32; P=0.033, OR = 2.64; 95% CI = 1.44–4.82, P=0.024, and OR = 2.79; 95% CI = 1.58–5.41; P=0.031, respectively). Interestingly, H. pylori vacA+/babA2+/oipA+ genotype infection was associated with increased risk of gastric cancer (OR = 3.85, 95% CI = 1.67–5.77, P=0.014). Conclusion. In this present study, we reported on the virulence genes of H. pylori infection to reveal their association with increased risk of chronic gastritis, precancerous gastric lesions, and gastric cancer. Precancerous gastric lesions with H. pylori vacA+/babA2+/oipA+ genotype increased the risk of gastric cancer.

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