scholarly journals Helicobacter pylori virulence factors and host genetic polymorphisms in a low gastric cancer and high Helicobacter Pylori prevalence country

GastroHep ◽  
2021 ◽  
Author(s):  
Colin J Rush ◽  
Ebrahim Hoosein ◽  
Nico de Villiers ◽  
Cornelis Clay ◽  
David C Metz ◽  
...  
Cells ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 27
Author(s):  
Jacek Baj ◽  
Alicja Forma ◽  
Monika Sitarz ◽  
Piero Portincasa ◽  
Gabriella Garruti ◽  
...  

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.


2013 ◽  
Vol 45 ◽  
pp. S60
Author(s):  
S. Zanussi ◽  
M. Casarotto ◽  
V. Canzonieri ◽  
G. Basaglia ◽  
V. De Re ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Tran Thi Huyen Trang ◽  
Seiji Shiota ◽  
Miyuki Matsuda ◽  
Tran Thanh Binh ◽  
Rumiko Suzuki ◽  
...  

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.


2013 ◽  
Vol 144 (5) ◽  
pp. S-324 ◽  
Author(s):  
Renato Cannizzaro ◽  
Stefania Zanussi ◽  
Vincenzo Canzonieri ◽  
Giancarlo Basaglia ◽  
Valli De Re ◽  
...  

Gut and Liver ◽  
2008 ◽  
Vol 2 (1) ◽  
pp. 23-29 ◽  
Author(s):  
Jung Mook Kang ◽  
Nayoung Kim ◽  
Sung-Il Cho ◽  
Dong Ho Lee ◽  
Young Soo Park ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Bruna Maria Roesler ◽  
Sandra Cecília Botelho Costa ◽  
José Murilo Robilotta Zeitune

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.


Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1293
Author(s):  
Ting-Yu Lin ◽  
Wen-Hsi Lan ◽  
Ya-Fang Chiu ◽  
Chun-Lung Feng ◽  
Cheng-Hsun Chiu ◽  
...  

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.


Toxins ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 677 ◽  
Author(s):  
Shamshul Ansari ◽  
Yoshio Yamaoka

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.


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