scholarly journals Statins’ Regulation of the Virulence Factors of Helicobacter pylori and the Production of ROS May Inhibit the Development of Gastric Cancer

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1293
Author(s):  
Ting-Yu Lin ◽  
Wen-Hsi Lan ◽  
Ya-Fang Chiu ◽  
Chun-Lung Feng ◽  
Cheng-Hsun Chiu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Virulence Factors ◽  
Treatment Strategies ◽  
Vacuolating Cytotoxin ◽  
Cholesterol Levels ◽  
Cytotoxin Associated Gene A ◽  
H Pylori ◽  
Cellular Components ◽  
Development Of Gastric Cancer

Conventionally, statins are used to treat high cholesterol levels. They exhibit pleiotropic effects, such as the prevention of cardiovascular disease and decreased cancer mortality. Gastric cancer (GC) is one of the most common cancers, ranking as the third leading global cause of cancer-related deaths, and is mainly attributed to chronic Helicobacter pylori infection. During their co-evolution with hosts, H. pylori has developed the ability to use the cellular components of the host to evade the immune system and multiply in intracellular niches. Certain H. pylori virulence factors, including cytotoxin-associated gene A (CagA), vacuolating cytotoxin A (VacA), and cholesterol-α-glucosyltransferase (CGT), have been shown to exploit host cholesterol during pathogenesis. Therefore, using statins to antagonize cholesterol synthesis might prove to be an ideal strategy for reducing the occurrence of H. pylori-related GC. This review discusses the current understanding of the interplay of H. pylori virulence factors with cholesterol and reactive oxygen species (ROS) production, which may prove to be novel therapeutic targets for the development of effective treatment strategies against H. pylori-associated GC. We also summarize the findings of several clinical studies on the association between statin therapy and the development of GC, especially in terms of cancer risk and mortality.

scholarly journals Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 1055 ◽  
Author(s):  
Jacek Baj ◽  
Izabela Korona-Głowniak ◽  
Alicja Forma ◽  
Amr Maani ◽  
Elżbieta Sitarz ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Epithelial Mesenchymal Transition ◽  
Treatment Strategies ◽  
Gastric Ulcers ◽  
Heparin Binding ◽  
Human Pathogens ◽  
Mesenchymal Transition ◽  
Cytotoxin Associated Gene A ◽  
H Pylori

Helicobacter pylori (H. pylori) is one of the most common human pathogens, affecting half of the world’s population. Approximately 20% of the infected patients develop gastric ulcers or neoplastic changes in the gastric stroma. An infection also leads to the progression of epithelial–mesenchymal transition within gastric tissue, increasing the probability of gastric cancer development. This paper aims to review the role of H. pylori and its virulence factors in epithelial–mesenchymal transition associated with malignant transformation within the gastric stroma. The reviewed factors included: CagA (cytotoxin-associated gene A) along with induction of cancer stem-cell properties and interaction with YAP (Yes-associated protein pathway), tumor necrosis factor α-inducing protein, Lpp20 lipoprotein, Afadin protein, penicillin-binding protein 1A, microRNA-29a-3p, programmed cell death protein 4, lysosomal-associated protein transmembrane 4β, cancer-associated fibroblasts, heparin-binding epidermal growth factor (HB-EGF), matrix metalloproteinase-7 (MMP-7), and cancer stem cells (CSCs). The review summarizes the most recent findings, providing insight into potential molecular targets and new treatment strategies for gastric cancer.

scholarly journals The Prevalence ofHelicobacter pyloriVirulence Factors in Bhutan, Vietnam, and Myanmar Is Related to Gastric Cancer Incidence

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Tran Thi Huyen Trang ◽  
Seiji Shiota ◽  
Miyuki Matsuda ◽  
Tran Thanh Binh ◽  
Rumiko Suzuki ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Virulence Factors ◽  
Cancer Incidence ◽  
The Status ◽  
The Difference ◽  
H Pylori ◽  
Significant Health ◽  
Development Of Gastric Cancer

Gastric cancer is a significant health problem in Asia. Although the prevalence ofHelicobacter pyloriinfection is similar in Bhutan, Vietnam, and Myanmar, the incidence of gastric cancer is highest in Bhutan, followed by Vietnam and Myanmar. We hypothesized thatH. pylorivirulence factors contribute to the differences. The status ofcagA,vacA,jhp0562, andβ-(1,3)galT(jhp0563)was examined in 371H. pylori-infected patients from Bhutan, Vietnam, and Myanmar. Each virulence factor could not explain the difference of the incidence of gastric cancer. However, the prevalence of quadruple-positive forcagA,vacAs1,vacAm1, andjhp0562-positive/β-(1,3)galT-negative was significantly higher in Bhutan than in Vietnam and Myanmar and correlated with gastric cancer incidence. Moreover, gastritis-staging scores measured by histology of gastric mucosa were significantly higher in quadruple-positive strains. We suggest that thecagA,vacAs1,vacAm1, andjhp0562-positive/β-(1,3)galT-negative genotype may play a role in the development of gastric cancer.

scholarly journals Helicobacter pylori Virulence Factors—Mechanisms of Bacterial Pathogenicity in the Gastric Microenvironment

Cells ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 27
Author(s):  
Jacek Baj ◽  
Alicja Forma ◽  
Monika Sitarz ◽  
Piero Portincasa ◽  
Gabriella Garruti ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Virulence Factors ◽  
Premalignant Lesions ◽  
Bacterial Pathogenicity ◽  
Current State ◽  
Genetic And Environmental Factors ◽  
H Pylori ◽  
Stimulation Of

Gastric cancer constitutes one of the most prevalent malignancies in both sexes; it is currently the fourth major cause of cancer-related deaths worldwide. The pathogenesis of gastric cancer is associated with the interaction between genetic and environmental factors, among which infection by Helicobacter pylori (H. pylori) is of major importance. The invasion, survival, colonization, and stimulation of further inflammation within the gastric mucosa are possible due to several evasive mechanisms induced by the virulence factors that are expressed by the bacterium. The knowledge concerning the mechanisms of H. pylori pathogenicity is crucial to ameliorate eradication strategies preventing the possible induction of carcinogenesis. This review highlights the current state of knowledge and the most recent findings regarding H. pylori virulence factors and their relationship with gastric premalignant lesions and further carcinogenesis.

scholarly journals Helicobacter Pylori Induce Gastric Upset

2021 ◽  
pp. 1-1
Author(s):  
Hazim Abdul Rahman Alhit
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Serum Antibody ◽  
Endoscopic Biopsy ◽  
Helicobacter Pylori Infection ◽  
Gastric Epithelium ◽  
Gastric Diseases ◽  
Heterogeneous Distribution ◽  
Cytotoxin Associated Gene A ◽  
H Pylori

Editorial: Helicobacter pylori is a micro-aerophilic, helical-form gramnegative aggressive bacteria. Accordingly, the idiom “Helico” intimates its helical appearance, “bacter” symbolizes bacteria, while “pylori” denotes stomach due to the first and common site of this bacteria living. Further, Marshall B. and Warren R. observed and described it in 1982. Then, the followed investigators studied this bacterium in detail with its consequences and complexities [1]. Gastric upset (Indigestion), dyspepsia: means impaired gastric digestion. Accordingly, the patient complains of upper abdominal pain, heartburn, belching, nausea, even feeling earlier gastric fullness than expected while eating. Furthermore, there are many causes of indigestion like gastroesophageal reflux disease, ulcer disease, gastritis, and even gastric cancer. Hence, unexplained recent onset dyspepsia in older people may need additional examinations. Moreover, one of the common causes is Helicobacter pylori infection, which needs laboratory and endoscopic examination [2]. Argument Many theories investigated the etiology and pathogenesis of Helicobacter pylori infection, concerning chronic or acute gastritis. Hence, gastric upset is the main presentation of both types of gastritis. Evidences The genotype is valuable in determining the dominant Helicobacter pylori strains as the isolates were different genetically plus heterogeneous distribution. Accordingly, the vac and cag markers operate a significant function in defining clinical consequences. These virulence agents are present in a subset of Helicobacter pylori strains isolates like cagA, iceA, vacA, and ureC. Moreover, the cagA causes cytotoxins induction by the gastric epithelial cell as Interleukin 8 [3]. The molecular intercommunication researches exhibit that the act of acarus calamus in hindering biofilm formation in Helicobacter pylori is due to the inhibitory impact of phytobio-active component, β-sitosterol, on the quorum sensing molecules-ToxB, PhnB, DnaA, plus Sip. Consequently, this opinion may suggest the molecular mechanism of Helicobacter pylori in producing the acidrelated complaints and gives a clue to a new therapy [4]. Helicobacter pylori infection causes lncRNA risk impression linked to H. pylori in gastric cancer patients and can prognosticate the prediction of these patients [5]. There was a close relationship between raised serum IgE levels in Helicobacter pylori infected patients [6]. Counterargument The laboratory investigations of Helicobacter pylori infection depend on several factors like the fluctuations of serum antibody titers in a time series, the antigene detection in stool tests, the false-positive results of lab tests, or the manner of endoscopic biopsy collection. Furthermore, other factors like the variations in Cytotoxin-Associated Gene A (CagA) in East Asian patients. Moreover, the gastric nodularity or atrophy, the patient’s age, the severity of the gastric mucosal infection are causes of variations in Helicobacter pylori detection at the time of the investigation [7]. Refutation The significant markers of H. pylori, the presence of the vacuolating cytotoxin (vacA), the cytotoxin-associated gene A (cagA), which induced by the direct communication with gastric epithelium factor antigen (iceA gene), and the presence of urease C gene (ureC). Consequently, all these factors play the principal factors in deciding the gastric consequences of Helicobacter infections. Conclusion Helicobacter pylori induce gastric upset by several mechanisms to form numerous Gastric diseases.

Evaluation of the Epidemiologic Efficacy of Eradicating Helicobacter pylori on Development of Gastric Cancer

2019 ◽  
Vol 41 (1) ◽  
pp. 97-108 ◽  
Author(s):  
Fujiao Duan ◽  
Chunhua Song ◽  
Jintao Zhang ◽  
Peng Wang ◽  
Hua Ye ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Population Attributable Risk ◽  
Eradication Therapy ◽  
Attributable Risk ◽  
Chinese Patients ◽  
Controlled Trials ◽  
Mixed Effect ◽  
H Pylori ◽  
Development Of Gastric Cancer

Abstract Eradication of Helicobacter pylori colonization has been reported to affect the progression of gastric cancer. A comprehensive literature search was performed from 1997 to 2017 using electronic databases. All randomized controlled trials (RCTs) and nonrandomized controlled trials (non-RCT) evaluated the effect of H. pylori eradication on development of gastric cancer. Four RCTs and 9 non-RCTs were included (n = 40,740 participants; 321,269 person-years). Overall, H. pylori eradication therapy was associated with a significantly reduced risk of gastric cancer (incidence rate ratio (IRR) = 0.52, 95% confidence interval (CI): 0.41, 0.65). Results of mixed-effect Poisson regression meta-analysis were similar to those of traditional meta-analyses. In stratified analyses, the IRRs were 0.59 (95% CI: 0.41, 0.86) in RCTs and 0.48 (95% CI: 0.36, 0.64) in non-RCTs. The IRRs were 0.45 (95% CI: 0.34, 0.61) in patients and 0.63 (95% CI: 0.44, 0.90) in the general population. Moreover, the relative risk reduction was approximately 77% on the development of noncardiac gastric cancer with H. pylori eradication therapy in China. Attributable risk percentage and population attributable risk percentage for Chinese patients were 77.08% and 75.33%, respectively, and for Japanese patients were 57.80% and 45.99%, respectively. H. pylori eradication therapy reduces the risk of noncardiac gastric cancer development. The findings indicate the importance of early intervention with H. pylori eradication therapy from the perspective of epidemiology.

scholarly journals Serum IgG antibodies against Helicobacter pylori low molecular weight antigens 50kDa, 30kDa and Urease A 26 kDa, along with vacuolating cytotoxin A are associated with the outcome of the infection

2020 ◽  
Vol 77 (4) ◽  
pp. 405-412
Author(s):  
Nebojsa Manojlovic ◽  
Ivana Tufegdzic ◽  
Elizabeta Ristanovic ◽  
Dubravko Bokonjic
Keyword(s):  
Gastric Cancer ◽  
Molecular Weight ◽  
Helicobacter Pylori ◽  
Functional Dyspepsia ◽  
Low Molecular Weight ◽  
Igg Antibodies ◽  
Vacuolating Cytotoxin ◽  
Specific Outcome ◽  
H Pylori ◽  
Topographic Distribution

Background/Aim. We designed and conducted this study due to the fact that results of the previous studies about seroreactivity to low-molecular-weight Helicobacter pylori antigens, cytotoxin-associated gene A (CagA), vacuolating cytotoxin A (VacA) in patients with gastric cancer and peptic ulcer were conflicting. Methods. The Western blot test was performed in 123 patients, 31 with gastric cancer, 31 with duodenal ulcer, 31 with gastric ulcer, 30 with gastritis and functional dyspepsia in order to determine IgG antibodies to H. pylori antigens (CagA, VacA, Heat shock protein 60kDa, Urease B 66 kDa, Flagellin 55kDa, 50kDa, 30 kDa, Urease A 26 kDa, 24 kDa). In this study we analyzed: seroreactivity to H. pylori antigens between group with functional dyspepsia and others; between grades of different histopathological parameters of inflammation of antral and corporal mucosa and between antrum-predominant gastritis and corpus-predominant gastritis + pangastritis groups. Results. It was shown that seropositivity to 50 kDa antigen could be used as a biomarker for functional dyspepsia, seropositivity to 30 kDa antigen for antrumpredominant gastritis and H. pylori colonization in the antrum, to UreaseA26 kDa antigen for pangastritis and corpus-predominant gastritis and degree of inflammation in the corpus. Seropositivity to VacA was the biomarker for gastric cancer and peptic ulcer taken together and inflammation of antral mucosa. Seropositivity to CagA was associated with more intensive inflammation of antral and corporal mucosa, Urease B66 kDa with inflammation of corpus mucosa, but neither of them with specific outcome of H. pylori infection and topographic distribution of gastric inflammation. Conclusion. Serum IgG antibodies to H. pylori antigens 50kDa, and VacA may represent useful biomarkers for the specific outcome of H. pylori infection, while serum antibodies to 30 kDa and UreaseA26 kDa antigens might be used as specific biomarkers for different topographic distribution of inflammation in gastric mucosa.

scholarly journals Gastric xanthelasma: case report

2020 ◽  
Vol 7 (2) ◽  
pp. 594
Author(s):  
Ana C. Almeida ◽  
Emília C. Fraga ◽  
Cristina P. Camacho ◽  
Maria J. Amaral ◽  
António Milheiro ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Case Report ◽  
Predictive Marker ◽  
Gastric Antrum ◽  
Complete Regression ◽  
Upper Gi ◽  
H Pylori ◽  
Single Lesion ◽  
Development Of Gastric Cancer

Xanthelasma, also known as Xanthoma or lipid island, is an uncommon gastrointestinal tract (GIT) tumor-like lesion and the stomach is its most frequent location in upper GI lesions, specifically in the gastric antrum, as a single lesion. The pathogenesis appears to be related to healing processes in response to tissue damage provoked by inflammation induced by Helicobacter pylori infection. Many studies have reported that successful H. pylori eradication helps prevent gastric cancer (GC) development. We present a case of a 77 years old patient that showed endoscopic diagnosis of erythematous gastropathy, a gastric antrum xanthelasma and H. Pylori infection. After confirmed H. pylori eradication, the lesion had complete regression. The successful eradication of H. pylori probably led to a total regression of the lesion. Gastric xanthelasma (GX) has been shown to be an independent predictive marker for early GC detection after H. pylori eradication. GX could be a useful marker for predicting the development of gastric cancer.

scholarly journals Differential Helicobacter pylori Plasticity in the Gastric Niche of Subjects at Increased Gastric Cancer Risk

Pathogens ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 65
Author(s):  
Mariateresa Casarotto ◽  
Chiara Pratesi ◽  
Ettore Bidoli ◽  
Stefania Maiero ◽  
Raffaella Magris ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Precancerous Lesions ◽  
Neutrophil Infiltration ◽  
Host Bacterium ◽  
Gastric Cancer Risk ◽  
Increased Risk ◽  
Cytotoxin Associated Gene A ◽  
Sydney System ◽  
H Pylori

Helicobacter pylori (H. pylori) represents an independent risk factor for Gastric Cancer (GC). First Degree Relatives (FDR) of GC subjects and Autoimmune Gastritis (AG) patients are both at increased risk for GC. H. pylori genetic heterogeneity within the gastric niche of FDR and AG individuals has been little explored. To understand whether they exploit an increased H. pylori stability and virulence, 14 AG, 25 FDR, 39 GC and 13 dyspeptic patients (D) were investigated by a cultural PCR-based approach characterizing single colonies-forming-units. We chose three loci within the Cytotoxin-associated gene-A Pathogenicity Island (CagPAI) (cagA,cagE,virB11), vacA, homA and homB as markers of virulence with reported association to GC. Inflammatory/precancerous lesions were staged according to Sydney System. When compared to D, FDR, similarly to GC patients, were associated to higher atrophy (OR = 6.29; 95% CI:1.23–31.96 in FDR; OR = 7.50; 95% CI:1.67–33.72 in GC) and a lower frequency of mixed infections (OR = 0.16; 95% CI:0.03–0.81 in FDR; OR = 0.10; 95% CI:0.02–0.48 in GC). FDR presented also an increased neutrophil infiltration (OR = 7.19; 95% CI:1.16–44.65). Both FDR and GC carried a higher proportion of CagPAI+vacAs1i1mx+homB+ profiles (OR = 2.71; 95% CI: 1.66–4.41 and OR = 3.43; 95% CI: 2.16–5.44, respectively). Conversely, AG patients presented a lower frequency of subtypes carrying a stable CagPAI and vacAs1i1mx. These results underline different H. pylori plasticity in FDR and AG individuals, and thus, a different host-bacterium interaction capacity that should be considered in the context of eradication therapies.

scholarly journals Recent Advances inHelicobacter pyloriInfection in Children: From the Petri Dish to the Playgound

2003 ◽  
Vol 17 (7) ◽  
pp. 448-454 ◽  
Author(s):  
Peng-Yuan Zheng ◽  
Nicola L Jones
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Petri Dish ◽  
Host Factors ◽  
Causative Role ◽  
Ulcer Disease ◽  
Recent Advances ◽  
H Pylori ◽  
Development Of Gastric Cancer

Helicobacter pyloriinfection is acquired in childhood, plays a causative role in chronic gastritis and peptic ulcer disease, and is associated with the development of gastric cancer. The present review focuses on recent advances in the scientific knowledge ofH pyloriinfection in children, including clinical sequelae, diagnosis and treatment. In addition, recent insights regarding both bacterial and host factors that mediate human diseases associated withH pyloriinfection are discussed.

scholarly journals Eradication Treatment of Helicobacter pylori Infection: Its Importance and Possible Relationship in Preventing the Development of Gastric Cancer

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Bruna Maria Roesler ◽  
Sandra Cecília Botelho Costa ◽  
José Murilo Robilotta Zeitune
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Genetic Factors ◽  
Salt Intake ◽  
Mucosal Damage ◽  
Bacterial Virulence ◽  
Host Genetic ◽  
H Pylori ◽  
Host Genetic Factors ◽  
Development Of Gastric Cancer

Helicobacter pylori is the most important carcinogen for gastric adenocarcinoma. Bacterial virulence factors are essential players in modulating the immune response involved in the initiation of carcinogenesis in the stomach; host genetic factors contribute to the regulation of the inflammatory response and to the aggravation of mucosal damage. In terms of environmental factors, salt intake and smoking contribute to the development of lesions. Various therapeutic schemes are proposed to eradicate H. pylori infection, which could potentially prevent gastric cancer, offering the greatest benefit if performed before premalignant changes of the gastric mucosa have occurred.

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