Abstract
In order to better understand pathogenicity of Helicobacter pylori, particularly in the context of its carcinogenic activity, we analysed expression of virulence genes: cagA, virB/D complex (virB4, virB7, virB8, virB9, virB10, virB11, virD4) and vacA in strains of the pathogen originating from persons with gastric diseases. The studies were conducted on 42 strains of H. pylori isolated from patients with histological diagnosis of non-atrophic gastritis—NAG (group 1, including subgroup 1 containing cagA+ isolates and subgroup 2 containing cagA- strains), multifocal atrophic gastritis—MAG (group 2) and gastric adenocarcinoma—GC (group 3). Expression of H. pylori genes was studied using microarray technology. In group 1, in all strains of H. pylori cagA+ (subgroup 1) high expression of the gene as well as of virB/D was disclosed, accompanied by moderate expression of vacA. In strains of subgroup 2 a moderate expression of vacA was detected. All strains in groups 2 and 3 carried cagA gene but they differed in its expression: a high expression was detected in isolates of group 2 and its hyperexpression in strains of group 3 (hypervirulent strains). In both groups high expression of virB/D and vacA was disclosed. Our results indicate that chronic active gastritis may be induced by both cagA+ strains of H. pylori, manifesting high expression of virB/D complex but moderate activity of vacA, and cagA- strains with moderate expression of vacA gene. On the other hand, in progression of gastric pathology and carcinogenesis linked to H. pylori a significant role was played by hypervirulent strains, manifesting a very high expression of cagA and high activity of virB/D and vacA genes.
Highlights
The causal relationship between bacterial pathogen of H. pylori and various forms of gastric disease, including gastric cancer (GC) has been well known
Considering the above, this study aimed at analysis of gene expression manifested by cagPAI and by vacA in Helicobacter pylori strains isolated from patients with non-atrophic gastritis, atrophic gastritis or gastric cancer
In studies on strains isolated from patients with non-atrophic gastritis (NAG) no principal differences could be disclosed in gastric histopathology, which could be linked to manifestation of cagA+ and cagA- strains
Summary
The causal relationship between bacterial pathogen of H. pylori and various forms of gastric disease, including gastric cancer (GC) has been well known. CagA, peptidoglycan and possible other bacterial factors become translocated to epithelial cells with mediation of type IV secretion system–T4SS, in contrast to cytotoxin VacA, belonging to the group of autotransporter proteins [4, 5]. The typical secretory apparatus type IV involves a syringe-like structure, coded by cagPAI virulence (vir) genes virB and virD4 [11, 12]. Products of the seven genes (virB4, virB7, virB8, virB9, virB10, virB11 and virD4) compose the so called VirB/D complex, forming secretory apparatus type IV (T4SS), recognised in Agrobacterium tumefaciens and Bordetella pertussis [13]. The VirB/D complex is indispensable to translocate bacterial toxin to eukaryotic cells [14]
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