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, 22 with gastric ulcer and 26 with chronic gastritis. Patients...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, 22 with gastric ulcer and 26 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-2 and TNF~ 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.展开更多
文摘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, 22 with gastric ulcer and 26 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-2 and TNF~ 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.
