Slomiany B L, Piotrowski J, Slomiany A
Research Center, University of Medicine and Dentistry of New Jersey, Newark 07103-2400, USA.
Biochem Mol Biol Int. 1998 Dec;46(5):1063-70. doi: 10.1080/15216549800204612.
Helicobacter pylori lipopolysaccharide is recognized as a primary virulence factor evoking acute mucosal inflammatory reaction associated with H. pylori infection. We investigated the activity of a key apoptotic protease, caspase-3, and the expression of inducible nitric oxide synthase (NOS-2) during H. pylori lipopolysaccharide-induced acute gastritis. The assays conducted 4 days following intragastric dose of the lipopolysaccharide revealed a pattern of acute mucosal responses characterized by an 11.2-fold increase in epithelial cells apoptosis, inflammatory infiltration of the lamina propria, hyperemia, and epithelial hemorrhage. This was accompanied by a 5.4-fold increase in caspase-3 activity, while the mucosal expression of NOS-2 showed a 6.5-fold induction. The results implicate H. pylori lipopolysaccharide in the induction of NOS-2 expression, and point to its effect on activation of the signaling cascade involving caspase-3 in the process gastric epithelial cells apoptosis.