Abstract
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.
Highlights
Helicobacter pylori, one of the most common bacteria to colonize the gastric epithelium of about half of the world’s population, has been estimated to accompany humans for at least 100,000 years [1].Based on epidemiological data, the bacterium has been categorized as a class-I carcinogen, because it is the strongest known risk factor for severe gastric complication development [2]
Once the permanent infection is established in the stomach, several gastro-duodenal complications like chronic gastritis, peptic ulcer diseases, gastric cancer, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma may develop [8]
It has been found that approximately 70% of all gastric ulcers and up to 80% of all duodenal ulcers are caused by H. pylori infection, which is a significant factor causing non-iatrogenic peptic ulcer diseases
Summary
Helicobacter pylori, one of the most common bacteria to colonize the gastric epithelium of about half of the world’s population, has been estimated to accompany humans for at least 100,000 years [1]. Once the permanent infection is established in the stomach, several gastro-duodenal complications like chronic gastritis, peptic ulcer diseases, gastric cancer, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma may develop [8]. The risk of peptic ulcer development increases with previous history of H. pylori infection even after its successful eradication compared with non-infected individuals [9]. Investigations indicate that the recurrence of peptic ulcer diseases decreases with the successful eradication of H. pylori infection compared to non-cured patients [10]. The development of gastric complications like peptic ulcer diseases and gastric cancer is a long-term process that may take several decades, and it is a multifactorial process influenced by gastric environmental, host genetic, and bacterial virulence factors [11]
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