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World J Gastroenterol. Sep 14, 2007; 13(34): 4610-4614
Published online Sep 14, 2007. doi: 10.3748/wjg.v13.i34.4610
Evidence for the role of gastric mucosa at the secretion of soluble triggering receptor expressed on myeloid cells (strem-1) in peptic ulcer disease
Vassilios Koussoulas, Spyridon Vassiliou, Ekaterini Spyridaki, Maria Demonakou, Ilia Vaki, Charalambos Barbatzas, Helen Giamarellou, Evangelos J Giamarellos-Bourboulis
Vassilios Koussoulas, Spyridon Vassiliou, Charalambos Barbatzas, Department of Gastroenterology, Sismanoglion General Hospital of Athens, University of Athens, Medical School, Greece
Ekaterini Spyridaki, Ilia Vaki, Helen Giamarellou, Evangelos J Giamarellos-Bourboulis, 4th Department of Internal Medicine, University of Athens, Medical School, Greece
Maria Demonakou, Department of Pathology, Sismanoglion General Hospital of Athens, University of Athens, Medical School, Greece
Author contributions: All authors contributed equally to the work.
Correspondence to: Vassilios Koussoulas, MD, Sismanoglion General Hospital, 1 Sismanogliou Str., Athens 15126, Greece. kous73@yahoo.gr
Telephone: +30-210-8039798 Fax: +30-210-8024454
Received: February 21, 2007
Revised: March 13, 2007
Accepted: March 21, 2007
Published online: September 14, 2007
Abstract

AIM: To investigate the role of gastric mucosa at the secretion of sTREM-1 in peptic ulcer.

METHODS: Seventy two patients were enrolled; 35 with duodenal, 21 with gastric ulcer and 16 with chronic gastritis. Patients were endoscoped and gastric juice was aspirated. Patients with duodenal and gastric ulcer underwent a second endoscopy post-treatment. Biopsies were incubated in the absence/presence of endotoxins or gastric juice. Supernatants were collected and sTREM-1 and TNFα were measured by enzyme immunoabsorbent assays. Scoring of gastritis was performed before and after treatment according to updated Sydney score.

RESULTS: Patients with duodenal and gastric ulcer and those with chronic gastritis had similar scores of gastritis. sTREM-1 was higher in supernatants of tissue samples of H pylori-positive than of H pylori-negative patients with gastric ulcer. Median (± SE) sTREM-1 was found increased in supernatants of patients with gastric ulcer before treatment (203.21 ± 88.91 pg/1000 cells) compared to supernatants either from the same patients post-treatment (8.23 ± 5.79 pg/1000 cells) or from patients with chronic gastritis (6.21 ± 0.71 pg/1000 cells) (P < 0.001 and < 0.001, respectively). Similar differences for sTREM-1 were recorded among LPS-stimulated tissue samples of patients (P = 0.001). Similar differences were not found for TNFα. Positive correlations were found between sTREM-1 of supernatants from patients with both duodenal and gastric ulcer before treatment and the degree of infiltration of neutrophils and monocytes.

CONCLUSION: sTREM-1 secreted by the gastric mucosa is an independent mechanism connected to the pathogenesis of peptic ulcer. sTREM-1 was released at the presence of H pylori from the inflamed gastric mucosa in the field of gastric ulcer.

Keywords: sTREM-1, Chronic gastritis, Gastric ulcer, Duodenal ulcer