These cytokines play many crucial roles in
H. pylori-associated gastritis through recruitment, activation, and infiltration of neutrophils into the sites of
infection as well as chronic inflammation and gastric
injury. Reactive oxygen and nitrogen species generated by activated inflammatory cells upon infection
can contribute to carcinogenesis through the formation
of DNA base lesions, such as 8-oxo-7,8-dihydro-20 -deoxyguanosine (8-oxodG), a marker of oxidative DNA
damage, resulting from G:C-to-T:A transversion. In
addition, 8-oxodG is remarkably increased in the gastric
epithelium of patients infected with H. pylori.