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AIM: To investigate interleukin-18 (IL-18) in patients with chronic panreatitis (CP). METHODS: We studied 29 patients with CP and 30 healthy controls. Peripheral blood mononuclear cells (PBMC) were isolated and incubated with 50 mmol/L ethanol, lipopolysaccharide (LPS) (doses 25 g/L, 250 g/L, 2500 g/L) and both agents for 24 h. Levels of IL-18 in the supernatants, and levels of IL-18, IL-12, interferon (IFN)-γ and soluble CD14 in the serum were analysed by ELISA technique. Expression of IL-18 in PBMC was investigated by reverse-transcription (RT)-PCR. IL-18 protein levels in CP tissue and in normal pancreas were studied by ELISA technique. IL-18 levels in PBMC and pancreatic tissue were determined by Westernblot. Im-munohistochemistry for pancreatic IL-18 expression was performed. RESULTS: In patients, IL-18 serum levels were signifi-cantly enhanced by 76% (mean: 289.9 ± 167.7 ng/L) compared with controls (mean: 165.2 ± 43.6 ng/L; P < 0.0005). IL-12 levels were enhanced by 25% in patients (18.3 ± 7.3 ng/L) compared with controls (14.7 ± 6.8ng/L, P = 0.0576) although not reaching the statistical significance. IFN-γ and soluble CD14 levels were not in-creased. In vitro, LPS stimulated significantly and dose-dependently IL-18 secretion from PBMC. Incubation with ethanol reduced LPS-stimulated IL-18 secretion by about 50%. The mRNA expression of IL-18 in PBMC and the response of PBMC to ethanol and LPS was similar in CP patients and controls. In PBMC, no significant differences in IL-18 protein levels were detected between patients and controls. IL-18 protein levels were increased in CP tissues compared to normal pancreatic tissues. IL-18 was expressed by pancreatic acinar cells and by infiltrating inflammatory cells within the pancreas. CONCLUSION: IL-18 originates from the chronically inflammed pancreas and appears to be involved in the fibrotic destruction of the organ.
METHODS: We studied 29 patients with CP and 30 healthy controls. Peripheral blood mononuclear cells (PBMC) were isolated and incubated with 50 mmol / L (IL-18) in patients with chronic pancreas Levels of IL-18 in the supernatants, and levels of IL-18, IL-12, IL-18, Interferon (IFN) -γ and soluble CD14 in the serum were analyzed by ELISA technique. Expression of IL-18 in PBMC was investigated by reverse-transcription (RT) -PCR. IL-18 protein levels in CP tissue and in normal pancreas were IL-18 levels in PBMC and pancreatic tissue were determined by Western blot. Im-munohistochemistry for pancreatic IL-18 expression was performed. RESULTS: In patients, IL-18 serum levels were signifi-cantly enhanced by 76% ( mean: 289.9 ± 167.7 ng / L) compared with controls (mean: 165.2 ± 43.6 ng / L; P <0.0005). IL-12 levels were enhanced by 25% in pa IFN-γ and soluble CD14 levels were not in-creased. In vitro, LPS stimulated significantly (P <0.05) Incubation with ethanol reduced LPS-stimulated IL-18 secretion by about 50%. The mRNA expression of IL-18 in PBMC and the response of PBMC to ethanol and LPS was similar in CP patients and controls. In PBMC, no significant differences in IL-18 protein levels were detected between patients and controls. IL-18 protein levels were increased in CP tissues compared to normal pancreatic tissues. IL-18 was expressed by pancreatic acinar cells and by infiltrating inflammatory cells within the pancreas. CONCLUSION: IL-18 originates from the chronically inflammed pancreas and appears to be involved in the fibrotic destruction of the organ.