Helicobacter pylori virulence genes

Abstract

Helicobacter pylori (H. pylori) is one of the most important human pathogens, infecting approximately half of the global population. Despite its high prevalence, only a subset of H. pylori infected individuals develop serious gastroduodenal pathology. The pathogenesis of H. pylori infection and disease outcome is thus thought to be mediated by an intricate interplay between host, environmental and bacterial virulence factors. H. pylori has adapted to the harsh milieu of the human stomach through possession of various virulence genes that enable survival of the bacteria in the acidic environment, movement towards the gastric epithelium, and attachment to gastric epithelial cells. These virulence factors enable successful colonization of the gastric mucosa and sustain persistent H. pylori infection, causing chronic inflammation and tissue damage, which may eventually lead to the development of peptic ulcers and gastric cancer. Numerous studies have focused on the prevalence and role of putative H. pylori virulence genes in disease pathogenesis. While several virulence factors with various functions have been identified, disease associations appear to be less evident, especially among different study populations. This review presents key findings on the most important H. pylori virulence genes, including several bacterial adhesins and toxins, in children and adults, and focuses on their prevalence, clinical significance and potential relationships.

Helicobacter pylori Related Diseases and Osteoporotic Fractures (Narrative Review)

“…The most studied virulence factors implicated in the pathogenicity of H.p. are produced by strains containing the following genes [ 29 , 31 ]: cytotoxin-associated gene A (cagA), vacuolating cytotoxin gene (vacA), duodenal ulcer (DU) promoting gene (dupA), induced by contact with epithelium gene (iceA), blood group antigen-binding adhesin (babA), sialic acid binding adhesin (sabA), outer inflammatory protein A (oipA), adherence-associated lipoprotein A and B (alpA/B), H.p. outer membrane protein Q (hopQ), gamma-glutamyl transpeptidase (GGT) and high-temperature requiring protein (HtrA).…”

Transformation of Helicobacter pylori into Coccoid Forms as a Challenge for Research Determining Activity of Antimicrobial Substances

“…The presence of this microorganism, however, is not neutral for the host, and is accompanied by the development of gastritis, which over the years may progress to gastric ulcers or cancers [2]. The appearance of these diseases is driven by an expression of a wide range of virulence factors, both adhesins and toxins [3]. Hence, the latest Maastricht V recommendations pointed to the necessity for the eradication of H. pylori infections, regardless of the presence of disease symptoms [4].…”

Using Probiotics as Supplementation for Helicobacter pylori Antibiotic Therapy

“…The prevalence of this gene was higher in strains from patients with duodenal ulcer than in those with gastritis or gastric cancer [48]. Data analysis have shown that individuals carrying dupA-positive strains are under increased risk for duodenal ulcers and gastric cancers [43].…”

“…After being injected into host cells through a type IV secretion system, CagA can interact with multiple host cell molecules, thus altering the intracellular signal transduction pathways of gastric epithelial cells to induce pro-inflammatory responses, leading to chronic inflammation of gastric mucosa. Meanwhile, CagA can facilitate carcinogenesis through the modulation of apoptosis, disruption of cell polarity, and promotion of genetic instability [43]. Apoptosis of gastric epithelial cells causes a decrease in gastric acid secretion and creates a more conducive environment for the H. pylori growth [44].…”