Involvement of endothelin-1 in up-regulation of gastric mucosal inflammatory responses to Helicobacter pylori lipopolysaccharide.
In this study, we investigated gastric mucosal inflammatory responses during Helicobacter pylori lipopolysaccharide-induced gastritis by analyzing the interplay between mucosal expression of endothelin-1 (ET-1), interleukin-4 (IL-4) and tumor necrosis factor-alpha (TNF-alpha). The assays conducted 4 days after intragastric dose of H. pylori lipopolysaccharide demonstrated a pattern of acute mucosal reaction characterized by the inflammatory infiltration of the lamina propria, hyperemia, and epithelial hemorrhage. This was accompanied by a 3.1-fold increase in the mucosal expression of ET-1 and a 9-fold enhancement in TNF-alpha, while the level of IL-4 showed a 20.8% decline. The results implicate ET-1 in gastric mucosal responses to H. pylori, and suggest that an increase in its level, combined with a loss of compensatory action by IL-4, may be responsible for the induction of TNF-alpha and triggering apoptotic events that exacerbate the inflammatory process.
Slomiany
B L
BL
Research Center, University of Medicine and Dentistry of New Jersey, Newark, New Jersey, 07103-2400, USA. slomiabr@umdnj.edu
Piotrowski
J
J
Slomiany
A
A
D000818:Animals; D019332:Endothelin-1 / Q000378:metabolism / Q000502:physiology*; D005753:Gastric Mucosa / Q000187:drug effects / Q000378:metabolism; D005756:Gastritis / Q000139:chemically induced*; D016480:Helicobacter pylori / Q000378:metabolism*; D018836:Inflammation Mediators / Q000378:metabolism*; D015847:Interleukin-4 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D019332:Endothelin-1; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D015847:Interleukin-4