Abstract
Gastric cancer is considered to be a type of gastrointestinal tumor and is mostly accompanied by Helicobacter pylori (HP) infection at the early stage. Hence, the long-term colonization of the gastric mucosa by HP as a causative factor for gastrointestinal diseases cannot be ignored. The virulence factors secreted by the bacterium activate the signaling pathway of oxidative stress and mediate chronic inflammatory response in the host cells. The virulence factors also thwart the antibacterial effect of neutrophils. Subsequently, DNA methylation is induced, which causes continuous cell proliferation and evolution toward low-grade-differentiated gastric cells. This process provides the pathological basis for the occurrence of progressive gastric cancer. Therefore, this review aims to summarize the oxidative stress response triggered by HP in the gastric mucosa and the subsequent signaling pathways. The findings are expected to help in the formulation of new targeted drugs for preventing the occurrence of early gastric cancer and its progression to middle and advanced cancer.
Highlights
The prevalence of infection by Helicobacter pylori (HP), a Gram-negative microaerobic bacterium, differs significantly between developed and developing countries (Fock and Ang, 2010)
To prevent the development of gastric diseases triggered by HP infection at an early stage, it is critical to understand the pathogenic mechanism of HP in the gastric host cells (GHCs)
The virulence factors of HP play a significant role in destroying the GHCs (Parker et al, 2010), such as cytotoxin-associated gene A (CagA), vacuolized cytotoxin (VacA; Backert and Clyne, 2011), the blood group antigen binding adhesion (BabA), etc
Summary
The prevalence of infection by Helicobacter pylori (HP), a Gram-negative microaerobic bacterium, differs significantly between developed and developing countries (Fock and Ang, 2010). The frequency of HP infection and the related diseases has demonstrated a decreasing trend in the Western countries, but it has shown an increasing trend every year with age in China, especially after the age of 10 years, which is closely related to the socioeconomic status and antibiotic resistance in China (Malfertheiner et al, 2017). Statistical data has demonstrated that HP infection occurs during childhood and develops into a hidden long-term infection or, later, into a variety of diseases. These diseases can be classified into internal and external gastrointestinal diseases. To prevent the development of gastric diseases triggered by HP infection at an early stage, it is critical to understand the pathogenic mechanism of HP in the gastric host cells (GHCs). We investigated the oxidative stress-mediated signaling pathway by virulence factor of HP, which provides theoretical guidance for the eradication of HP in combination with novel-targeted and other alternative therapies
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
