Abstract
BackgroundNumerous proteins have been proposed as virulence factors for the gram negative gastric bacterium Helicobacter pylori but only for a few this has unequivocally been demonstrated. The aim of the current study was to evaluate the association of the putative virulence factors tnpA and tnpB (no cagA) with H. pylori associated gastroduodenal diseases.MethodsA PCR based assay was used to determine the presence of the tnpA and tnpB genes, as well as of cagA, in 360H. pylori strains isolated from H. pylori infected patients.ResultsOf 360H. pylori culture positive patients (196 men, 164 women; average age 42.1 years (range 17–73), 95 had gastritis, 92 had gastric ulcers, 108 had duodenal ulcers, and 65 had gastric cancer. Using the gastritis group as a reference a significantly aberrant gene distribution was observed for the tnpA (Relative risk: 1.45; 95% CI 1.04-1.93), the cagA (Relative risk: 1.81; 95% CI 1.44-2.29), but not the tnpB gene in the gastric cancer group.ConclusionsThe increased incidence of the tnpA gene in gastric cancer patients suggests a role of the tnpA gene in the development of H. pylori induced gastric cancer.
Highlights
Numerous proteins have been proposed as virulence factors for the gram negative gastric bacterium Helicobacter pylori but only for a few this has unequivocally been demonstrated
Patients All patients suspect of a H. pylori infection that visited the Tooba Medical Center, in Sari, Iran for endoscopic examination between May 2008 and October 2010 were invited to participate in this study
376 patients suspect for H. pylori infection were enrolled, but H. pylori specific growth was not observed from the biopsy specimen in 16 of them
Summary
Numerous proteins have been proposed as virulence factors for the gram negative gastric bacterium Helicobacter pylori but only for a few this has unequivocally been demonstrated. Colonization always results in acute gastritis and chronic gastritis when left untreated [2] Additional complications such as gastric ulcers (GU), duodenal ulcers (DU), or gastric cancer (GC) may develop in some of these H. pylori infected patients [3]. The CagA protein is a commonly accepted virulence factor and the cagA gene is often used as a marker for the of the country [12,13] This high prevalence is coupled to an even higher rate of H. pylori induced peptic ulcer disease and gastric cancers [14]. This makes it an ideal geographically confined region to study the effect of genetic variation of this gastric pathogen on infection associated disorders. In this study we determined associations of the presence of tnpA and tnpB and clinical manifestations of H. pylori infections in patients from the North of Iran
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