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Induction of caspase‐3 and nitric oxide synthase‐2 during gastric mucosal inflammatory reaction to Helicobacter pylori lipopolysaccharide
Author(s) -
Slomiany B. L.,
Piotrowski J.,
Slomiany A.
Publication year - 1998
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216549800204612
Subject(s) - lipopolysaccharide , helicobacter pylori , nitric oxide synthase , lamina propria , apoptosis , nitric oxide , gastric mucosa , chemistry , gastritis , immunology , microbiology and biotechnology , biology , medicine , stomach , epithelium , pathology , biochemistry
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.