Abstract

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.

Highlights

  • Published: 3 December 2021Helicobacter pylori is a Gram-negative bacterium that selectively colonizes the gastric epithelium

  • Infection commonly results in chronic gastritis that eventually leads to intestinal metaplasia and dysplasia, which in turn culminate in the initiation of gastric cancer [3,4]

  • In H. pylori, it is encoded by the 40 kb genetic locus of cytotoxin-associated gene pathogenicity island, a portion of the chromosome that possesses different CG content and is usually acquired through horizontal transfer

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Summary

Introduction

Helicobacter pylori is a Gram-negative bacterium that selectively colonizes the gastric epithelium. A recent systemic review suggested a pooled prevalence of up to 17.4% of Helicobacter pylori-mediated gastric cancers among infected population [8]. In a systematic review conducted by Hooi, Lai [10], the highest prevalence of H. pylori was reported in Africa (70.1%), followed by South America (69.4%) and Western. This review discusses the unique bacterial characteristics helical shape, to produce urease, flagella movement, andThe outer membrane proteins that confer itsability successful survival within the stomach lumen. Upon reaching the gastric epithelium, H. ability toare produce flagella movement, and outer membrane proteins (OMPs) are pylori firmly to factors host cells viaUpon various. Reaching gastric epithelium, H. pylori attaches firmly to host cellsdetachment via various OMPs produces amovement permanent colonizing strainThen, to prevent strain prevent from and the peristaltic of the bowels.

Structure
OMPs Facilitate Bacterial Attachment to the Gastric Epithelial Cells
Type IV Secretion System Penetrates Gastric Epithelial Cells
CagA Perturbs Normal Cell Activities
VacA Induces Host Cell Vacuolation
Findings
Conclusions
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