Detection of virulence gene belonging to cag pathogenicity island in Helicobacter pylori isolates after multiple unsuccessful eradication therapy in Northwest Croatia

Abstract

Background: Some of the genes belonging to cag pathogenicity island (cagPAI) in Helicobacter pylori were found to be associated with an increased severity of gastric mucosal inflammation that might lead to the development of gastroduodenal disease. Aim: The aim of our study was to define a group of patients based on the frequency of virulence genes of cagPAI island and comparison with pathohistological alterations of gastric mucosa who need to be subjected to further eradication therapy after previous unsuccessful eradication therapy and in spite of benign endoscopic findings.Material and methods: In total 103 H. pylori isolates were analysed. Genes encoding virulence factors were detected by PCR with primers for 10 loci in cagPAI: Apcag (cagA promotor region), cagA1, cagA2, cagA3, cagM, cagT, cagE, LEC, tnpA and tnpB. The patients who provided isolates were classified into three clinical categories: non-ulcer dyspepsia (n=69), erosio/ulcus ventriculi (n=22) and erosio/ulcus duodeni (n=12 (5)(6). On the contrary, some of the authors did not find correlation between cagPAI and gastroduodenal disease (7). CagPAI encodes multiple structural components of bacterial type IV secretion system (T4SS). T4SS translocates cagA protein directly to the cytosol of the gastric epitelium where it gets tyrosin phosphorylated by Src-family kinases and becomes able to alter the host cell functions leading to malignant transformation (2). CagA gene is located in the region I of cagPAI and is considered to be the marker of this region. CagA positive isolates are associated with more severe clinical features in many studies. However, there are contradictory results in the references regarding these studies.CagE is also located in the region I and is necessary to induce production of interleukin IL-8. Some authors consider cagE gene to be better marker of cagPAI region compared to cagA and more useful in monitoring the progress of H. pylori induced gastric disease. CagT gene is a marker of cagII region and some studies connect it with more severe clinical disease (8). LEC (left terminal end of cagII) is not necessary for translocation of cagA into the host cell or induction of interleukin IL8. It is associated with peptic ulcer and adenocarcinoma. Some of the study found connection of tnpA gene with peptic ulcer (9).There are no published studies on the presence of H. pylori virulence genes in Croatia. Considering quite large number of patients with multiple unsuccessful eradication therapy, in spite of lack of clinical symptoms and benign endoscopic result, there is a question to pose whether to insist on eradication or not.The aim of our study was to detect virulence genes of H. pylori just in these patients as a possible predictors of future severe gastroduodenal diseases, by comparing it with clinical and pathohistological results. MATERIAL AND METHODS PatientsThe study analysed gastroscopic test results and bioptic specimens of gastric mucosa with positive H. pylori culture in 103 patients examined during routine, clini...

The organization of Helicobacter pylori cag-pathogenicity island (cagPAI) genes in multiracial population with histopathological changes of gastric mucosa

“…In their study, few cagPAI genes (cagE, cagL, cagT and HP521) were examined to detect the intactness of cagPAI region. Discordant in the frequency of cagPAI intactness in many reports was due to the difference cagPAI genes that being examined [14,27,28]. Thus, results of the present study indicate that deletions can occur in all parts of the cagPAI and screening the entire genes in the cagPAI is needed to determine the accurate organization of the cagPAI region.…”