Influence of cagA and Helicobacter pylori infection on serum oxidative DNA damage in patients with peptic ulcer disease

Helicobacter pylori (H. pylori) infection is one of the most common gastrointestinal infections worldwide. Infection with H. pylori strains cause in different pathological manifestation and increased oxidative stress leads to a strong inflammatory response in gastric mucosa. There is continuing interest in identifying H. pylori virulence factors that might predict the risk for symptomatic clinical outcomes. The prevalence of cagA gene, protein and the association of serum levels of 8-hydroxy-2-deoxyguanosine (8-OHdG) with oxidative DNA damage were determined. The presence of IgG antibody against CagA protein was determined by using Western blotting technique. The presence of cagA gene was examined by PCR. Oxidative DNA damage status was determined using serum levels of 8-OHdG. Biopsies were considered as H. pylori-positive and negative when both the rapid urease test and bacterial culture gave positive and negative results respectively. H. pylori-positive and cagA-positive was predominant in all clinical outcomes. There was no significant association between prevalence of CagA status and clinical outcomes. The serum levels of 8-OHdG was at a higher level in H. pylori-positive patients. Our results suggest that cagA-positive strains were predominant in patients. However, we found no association between cagA status and clinical outcomes and this virulence factor is not associated with the development of PUD. In addition, serological tests such as the western blotting are helpful in detecting subjects infected with H. pylori strains in PUD and NUD. H. pylori infection may be associated with increased serum 8-OHdG.