Abstract
Helicobacter pylori (H. pylori) plays a crucial role in the pathogenesis of gastritis, peptic ulcer, and gastric cancer. The presence of pathogenicity islands (PAI) genes contributes to the pathogenesis of many gastrointestinal disorders. Cytotoxin-associated gene A (cagA) and vacuolating cytotoxin gene (vacA) are the most known virulence genes in H. pylori. So, our aim was to study H. pylori virulence genes' role in gastric disorders pathogenesis. Our study included 150 adult patients who suffered dyspeptic symptoms and were referred to the GIT endoscopy unit. Gastric biopsies were attained for rapid urease test (RUT) and histopathological examination, and multiplex PCR technique for detection of virulence genes was performed. It was found that 100 specimens were (RUT) positive, of which sixty samples (60%) were PCR positive for H. pylori ureC gene. The vacA and cagA genes were identified in 61.6% and 53% of H. pylori strains, respectively. Only 5 cases were vacA-positive and cagA-negative. The most virulent vacA s1 allele existed in 56.6% of cases. Out of the 60 H. pylori strains, 66% had at least one virulence gene and 34% did not show any virulence gene. H. pylori infection showed significant increase with age. H. pylori are prevalent amid dyspeptic patients in our region. The main genotype combinations were vacA+/cagA+ of s1m1 genotype and they were frequently associated with peptic ulcer diseases, gastritis, and gastroesophageal reflux disease.
Highlights
H. pylori infection causes Peptic Ulcer Disease (PUD) and Gastric Carcinoma (GC) and affects almost half of the world’s population [1]
We studied H. pylori virulence genes in infected patients suffering from dyspepsia after gastric biopsy and the association between those genes and endoscopic findings detected
Antral gastritis was the most predominant endoscopic finding followed by Gastroesophageal Reflux Disease (GERD) and pangastritis (36.6%, 34%, and 26.6%, respectively)
Summary
H. pylori infection causes Peptic Ulcer Disease (PUD) and Gastric Carcinoma (GC) and affects almost half of the world’s population [1]. H. pylori virulent strains and the host genetic condition were blamed for a wide variety of gastric disorders. H. pylori virulence genes encode the proteins which are responsible for damaging the gastric epithelium. E H. pylori pathogenicity island (PAI) was initially known as cytotoxin-associated gene (cag), since it was assumed to be related to expression of the vacuolating toxin (vacA). It was afterwards demonstrated that both factors, vacA and the PAI, are separate of each other, even though cag-negative strains often do not express vacA [2]. E pathogenicity island (cagA-PAI) is found in the most virulent H. pylori strains. CagA-PAI is about 40 kb region, containing 31 genes that encode a type IV secretion system, related to cagA translocation and the host’s inflammatory response [3]. CagA encodes a 120–145 kDa immunodominant protein and is placed at the end of the cagA-PAI [4]
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