期刊
MICROORGANISMS
卷 9, 期 12, 页码 -出版社
MDPI
DOI: 10.3390/microorganisms9122502
关键词
Helicobacter pylori; flagella; outer membrane protein; CagA; VacA; type IV secretion system; pathogenesis
类别
资金
- Malaysia Ministry of Higher Education Fundamental Research Grant Scheme [FP133-2019A]
- Institut Merieux Young Investigator Fund [IF039-2017]
- Malaysia Public Service Department
Helicobacter pylori, armed with unique virulence factors, is capable of surviving in the harsh stomach environment and causing inflammation and tissue damage, leading to gastric cancer. The bacterium not only establishes colonization in the stomach, but also manipulates the host immune system to ensure long-term survival.
Helicobacter pylori is well established as a causative agent for gastritis, peptic ulcer, and gastric cancer. Armed with various inimitable virulence factors, this Gram-negative bacterium is one of few microorganisms that is capable of circumventing the harsh environment of the stomach. The unique spiral structure, flagella, and outer membrane proteins accelerate H. pylori movement within the viscous gastric mucosal layers while facilitating its attachment to the epithelial cells. Furthermore, secretion of urease from H. pylori eases the acidic pH within the stomach, thus creating a niche for bacteria survival and replication. Upon gaining a foothold in the gastric epithelial lining, bacterial protein CagA is injected into host cells through a type IV secretion system (T4SS), which together with VacA, damage the gastric epithelial cells. H. pylori does not only establishes colonization in the stomach, but also manipulates the host immune system to permit long-term persistence. Prolonged H. pylori infection causes chronic inflammation that precedes gastric cancer. The current review provides a brief outlook on H. pylori survival tactics, bacterial-host interaction and their importance in therapeutic intervention as well as vaccine development.
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