Relationship between ureB Sequence Diversity, Urease Activity and Genotypic Variations of Different Helicobacter pylori Strains in Patients with Gastric Disorders

Abstract

A b s t r a c tAssociation of the severity of Helicobacter pylori induced diseases with virulence entity of the colonized strains was proven in some studies. Urease has been demonstrated as a potent virulence factor for H. pylori. The main aim of this study was investigation of the relationships of ureB sequence diversity, urease activity and virulence genotypes of different H. pylori strains with histopathological changes of gastric tissue in infected patients suffering from different gastric disorders. Analysis of the virulence genotypes in the isolated strains indicated significant associations between the presence of severe active gastritis and cagA + (P = 0.039) or cagA/iceA1 genotypes (P = 0.026), and intestinal metaplasia and vacA m1 (P = 0.008) or vacA s1/m2 (P = 0.001) genotypes. Our results showed a 2.4-fold increased risk of peptic ulcer (95% CI: 0.483-11.93), compared with gastritis, in the infected patients who had dupA positive strains; however this association was not statistically significant. The results of urease activity showed a significant mean difference between the isolated strains from patients with PUD and NUD (P = 0.034). This activity was relatively higher among patients with intestinal metaplasia. Also a significant association was found between the lack of cagA and increased urease activity among the isolated strains (P = 0.036). While the greatest sequence variation of ureB was detected in a strain from a patient with intestinal metaplasia, the sole determined amino acid change in UreB sequence (Ala201Thr, 30%), showed no influence on urease activity. In conclusion, the supposed role of H. pylori urease to form peptic ulcer and advancing of intestinal metaplasia was postulated in this study. Higher urease activity in the colonizing H. pylori strains that present specific virulence factors was indicated as a risk factor for promotion of histopathological changes of gastric tissue that advance gastric malignancy. K e y w o r d s: Helicobacter pylori, virulence, factor urease activity, histopathological changes

Helicobacter pylori Virulence Factors—Mechanisms of Bacterial Pathogenicity in the Gastric Microenvironment

“…Moreover, urease and catalase activity, as well as protein synthesis by H. pylori , might be impaired at very low pH [ 27 ]. Greater urease activity might be associated with a higher risk of induction of the histopathological alterations within the gastric mucosa and further gastric carcinogenesis [ 28 ]. Urease activity might be modulated by the flbA gene, the same gene that is involved in flagellar biosynthesis [ 29 ].…”

Prevalence of non Helicobacter pylori gastric Helicobacters in Iranian dyspeptic patients

“…Up to now, more than 30 species have been characterized and well-recognized by microbiologists. H. pylori is the most recognized bacterium associated with dyspepsia in humans [1][2][3][4]. However, NHPGH species with typical spiral morphology has the ability to colonize the stomach of humans and animals.…”

Characterization of Specific IgA Response to Antigenic Determinants ofHelicobacter pyloriUrease Encoded byureAandureBin Children

“…According to the report by Ghalehnoei et al, some variants of UreB could be shown depending on the strains (17). Thirty percent of patients with intestinal metaplasia showed a single amino acid sequence change in UreB, but this change did not affect the urease activity at all (17). As mentioned above, urease is a relatively conserved protein for H. pylori survival in stomach, and although it may have some changes depending on the strains, it does not seem to affect the function and activity of urease.…”

“…Urease, which hydrolyzes urea into NH3 and CO2, plays important role in H. pylori colonization in the acidic condition of stomach (pH 3) (10). According to the report by Ghalehnoei et al, some variants of UreB could be shown depending on the strains (17). Thirty percent of patients with intestinal metaplasia showed a single amino acid sequence change in UreB, but this change did not affect the urease activity at all (17).…”