The mechanism by which Helicobacter pylori, which has little or no invasive activity, induces gastric-tissue inflammation and injury has not been well characterized. Extensive research during the past 2 decades has revealed the mechanism by which continued oxidative stress can lead to chronic inflammation, which in turn could mediate most chronic diseases including gastritis. The present study is aimed to analyze the effect of H pylori Lipopolysaccharide LPS on immune system activation particularly oxidative stress. We have investigated the immunomodulatory effect of H. pylori LPS isolated from gastritis patients. LPS was challenged to neutrophils and macrophage, in response to which reactive oxygen species (ROS) and reactive nitrogen species (NO) were measured by chemiluminescence technique and spectrophotometry respectively. Additionally effect on T-cells proliferation was also studied by radioactive thymidine incorporation using scintillation counter. In this study, we have found that out of 10 different samples of H. Pylori LPS, 6 of the LPS samples resulted in 2-6 μM of NO nitric oxide production in vitro. About 3 samples were aggravating reactive oxygen species production and almost all the samples moderately inhibited proliferation of T cell. All these events modulated by LPS clearly indicating the role of bacterial lipopolysaccharide in an increased proinflammatory activity which may lead to gastritis.