Role of soluble triggering receptor expressed on myeloid cells in inflammatory bowel disease

AIM： To investigate the probable role of soluble triggering receptor expressed on myeloid cells-1 （sTREM-1） in the pathogenesis of inflammatory bowel disease （IBD）.METHODS： Fifty-eight patients were enrolled; nineteen healthy volunteers served as controls; 8 patients were diagnosed with Crohn＇s disease, and 31 with ulcerative colitis, Clinical and endoscopic activity indexes of patients with Crohn＇s disease and ulcerative colitis respectively were estimated, Upon admission blood was sampled; sTREM-1 and TNFα were measured by an immunoassay and malondialdehyde （IDA） by the thiobarbitourate assay, after passage through an HPLC system,RESULTS： Median ± SE of TNFα of controls, patients with Crohn＇s disease and patients with ulcerative colitis were 6.02 ± 3.94, 7.98 ± 5.08 （P = NS vs controls）, and 8.45 ± 4.15 ng/L （P = 0.018 vs controls） respectively. Respective values of sTREM-1 were 53.31 ± 32.93, 735.10 ± 197.17 （P = 0.008 vs controls） and 435.82 ± 279.71 ng/L （P = 0.049 vs controls）, sTREM-1 was positively correlated with Crohn＇s disease activity index and clinical and endoscopic activity indexes of ulcerative colitis （P = 0.002, 0.001 and 0.009, respectively）, sTREM-1 of patients with ulcerative colitis was positively correlated with TNFα （P = 0.001）.CONCLUSION： sTREM-1 seems to behave as a novel mediator in IBD in correlation with the degree of the intlammatory reaction of the intestinal mucosa.

Monocytes in systematic inflammatory response syndrome:Differences between sepsis and acute pancreatitis

AIM: To unravel the differences between systematic in- flammatory response syndrome (SIRS) of acute pancre- atitis compared to the same syndrome in sepsis. METHODS: Twenty-five patients were enrolled, 12 with sepsis and 13 acute pancreatitis. After diagnosis 20 ml blood was sampled. Half were assayed for isolation of monocytes and 10 ml was centrifuged for serum test of tumor necrosis factor alpha (TNFα) and interleukin-6 (IL-6). Half of monocytes were incubated in the presence of patients’ serum and supernatants were collected. The other half was treated for estimation of optical photom- etry under caspase-3 inhibition. TNFα and IL-6 were es- timated by an enzyme immunoassay. RESULTS: median ± SE of serum IL-6 in septic patients and acute pancreatitis patients was 192.30 ± 35.40 ng/L and 21.00 ± 16.05 ng/L, respectively (P < 0.01). Re- spective values of caspase-3 were 0.94 ± 0.17 pmol/min 104 cells and 0.34 ± 0.09 pmol/min 104 cells (P < 0.05). IL-6 of monocyte supernatants of patients with sepsis was significantly increased after addition of patients’ serum, while that of patients with acute pancreatitis did not show significant difference. CONCLUSION: The data have shown that monocyte activity is different between acute pancreatitis and sepsis. This phenomenon might be explained as a different pathway to the pro-inflammatory cytokines release or could be a novel anti-inflammatory response in acute pancreatitis.

Evidence for the role of gastric mucosa at the secretion of soluble triggering receptor expressed on myeloid cells(strem-1) in peptic ulcer disease

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.