NADPH and iron may have an important role in attenuated mucosal defense in Helicobacter pylori infection?

Host intracellular iron has been recognized as an important cofactor in induction of nicotinamide adenine dinucleotide phosphate (NADPH)-dependent oxidative burst as antimicrobial defense mechanism. It is plausible that iron chelator directly inactivates NADPH oxidase by chelating the active site heme iron of flavocytochrome b558 thus blocking the transfer of electrons from NADPH to oxygen and its reduction to superoxide anion. Thus, altering the equilibrium of intracellular iron could influence the course of infection to the enhancement of the pathogen with regard to oxidative stress.