Helicobacter pylori infection upregulates endothelial nitric oxide synthase expression and induces angiogenesis in gastric mucosa of dyspeptic patients.
BACKGROUND
Helicobacter pylori (H. pylori) infection induces nitric acid (NO) overproduction through inducible NO synthase (NOS) expression, subsequent DNA damage and enhanced antiapoptosis signal transduction sequence in the human gastric mucosa, whereas its possible effect on endothelial nitric oxide synthase (eNOS) expression has not as yet been investigated. The aim of this study was to evaluate the effect of H. pylori infection in the expression of eNOS in gastric mucosa.


METHODS
We prospectively studied 30 nonsmoking dyspeptic patients (12 men, 18 women, mean age 54.26+/-12.89 years). The diagnosis of H. pylori infection was based mainly on histology. The histological grading of H. pylori infection was evaluated according to the modified Sydney classification. Histological grading of eNOS expression and microvessel density as estimated by CD34 expression were determined by immunohistochemistry (degree 0-3) and correlated with H. pylori infection and histological degree of gastritis.


RESULTS
Twelve patients were H. pylori-positive and 18 patients were H. pylori-negative. The two groups were matched for age (P=0.139), sex (P=0.342) and similar degree of gastritis. Intensity of eNOS and CD34 expression in the corpus and antrum were significantly correlated (P<0.001). eNOS expression was correlated with H. pylori infection in the mucosa of the body and antrum (P=0.013 and 0.037, respectively) but not with gastric inflammation and activity (P=0.848 and 0.871, respectively, for the corpus and P=0.565 and 0.793, respectively, for the antrum). H. pylori-positive patients showed higher expression of CD34-positive blood vessels in the mucosa of the antrum (P=0.048). CD34 expression was correlated with gastric inflammation and activity (P=0.03 and 0.044, respectively) in the mucosa of the antrum of H. pylori-positive patients.


CONCLUSIONS
H. pylori infection upregulates eNOS, and induces angiogenesis, contributing to H. pylori-associated pathophysiology in gastric mucosa.
Lazaraki
Georgia
G
First Department of Internal Medicine, Gastroenterology Clinic, AHEPA University , Aristotle University of Thessaloniki, Thessaloniki, Greece. lazarakg@yahoo.com
Kountouras
Jannis
J
Metallidis
Simeon
S
Vrettou
Eleni
E
Tzioufa
Valentini
V
Germanidis
Georgios
G
Chatzopoulos
Dimitrios
D
Zavos
Christos
C
Giannoulis
Kleanthis
K
Nikolaidis
Paul
P
D000328:Adult; D000368:Aged; D018952:Antigens, CD34 / Q000378:metabolism; D004415:Dyspepsia / Q000201:enzymology / Q000382:microbiology / Q000473:pathology; D005260:Female; D005753:Gastric Mucosa / Q000098:blood supply* / Q000201:enzymology / Q000378:metabolism; D005756:Gastritis / Q000201:enzymology / Q000382:microbiology; D016481:Helicobacter Infections / Q000150:complications / Q000201:enzymology*; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000382:microbiology*; D052250:Nitric Oxide Synthase Type III / Q000096:biosynthesis*; D011446:Prospective Studies; D015854:Up-Regulation
D018952:Antigens, CD34; D052250:Nitric Oxide Synthase Type III