Prevalence of virulence genes and antigen pattern in H. pylori-infected patients and the level of some inflammatory cytokines compared with non-infected individuals
The worldwide prevalence of Helicobacter pylori is about 50%. This bacterium needs a number of virulence factors for pathogenesis. This study aimed to determine the prevalence of virulence genes (ureB, cytotoxin-associated gene A [cagA], and vacuolating cytotoxin [vacA]), as well as the antigenic profile in H. pylori strains.
Eighty-five patients with abdominal pain, including 46 H. pylori-positive (Hp+) and 39 H. pylori-negative (Hp-) cases, were enrolled in this study. The serum levels of interleukin (IL)-17F, tumor necrosis factor α (TNF-α), and interferon γ (IFN-γ) cytokines were measured by multiplex kits and flow cytometry. After molecular identification by the ureC gene, vacA, cagA, and ureB genes were detected by polymerase chain reaction (PCR). Finally, after antigenic extraction, the whole-cell protein was exhibited by sodium dodecyl sulphate–polyacrylamide gel electrophoresis (SDS-PAGE).
The prevalence of vacA, ureB, and cagA genes were 91.3%, 67.39%, and 50%, respectively. The frequency of genes and cell surface antigens were not significantly different based on the gastritis severity (p > 0.05). IL-17F significantly (p = 0.046) increased in the presence of 19.5 kDa (outer membrane protein [OMP]). Moreover, the OMP antigen significantly enhanced immunoglobulin A (IgA; p = 0.013). In the presence of the 66-kDa (ureB) antigen, the serum level of IFN-γ increased (p = 0.041). Finally, the CagA protein led to increased IgG antibody levels (p = 0.027).
Early detection of H. pylori infection can play a crucial role in managing it. Our results suggest that IL-17F, TNF-α, and IFN-γ cytokines could be diagnostic markers. However, further studies are required to fully investigate this suggestion.
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