AIM:To determine the tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6) and soluble interleukin 2 receptor (sIL-2r) from peripheral blood mononuclear cells (PBMC) in 25 Chinese patients with ulcerative colitis and 20 healthy controls. METHODS: PBMC were isolated by density gradient centrifugation of heparinized blood and cultures for 24 or 48 hours by stimulation with LPS or PHA. TNF-alphaand sIL-2r were measured by ELISA method and IL-6 measured by biossay. RESULTS: TNF-alphaproduction stimulated by LPS and sIL-2r production by PHA in ulcerative colitis were significantly lower than in healthy controls (TNF-alpha509(46-7244)ng/L vs 1995(117-18 950)ng/L, P < 0.05; sIL-2r 320U/mlplus minus 165U/ml vs 451U/mlplus minus 247U/ml, P < 0.05).Spontaneous TNF-alphaand sIL-2r production were not significantly different between ulcerative colitis and controls (TNF-alpha304(46-7044)ng/L vs 215(46-4009)ng/L,P > 0.05; sIL-2r 264U/mlplus minus 115U/ml vs 236U/mlplus minus139U/ml, P>0.05). IL-6 production by spontaneous release from PBMC in ulcerative colitis group was 109U/mlplus minus 94U/ml vs 44U/mlplus minus 39U/ml for those in healthy controls, P < 0.01. IL-6 stimulated by LPS in ulcerative colitis group was (261U/ml plus minus 80U/ml) higher than in healthy controls (102U/mlplus minus 54U/ml, P < 0.01). No correlation of TNF-alpha, IL-6, sIL-2r production was found to disease activity, disease location and medication. CONCLUSION: Cytokine production from PBMC was also disturbed in Chinese patients with ulcerative colitis.
AIM:To determine the tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6) and soluble interleukin 2 receptor (sIL-2r) from peripheral blood mononuclear cells (PBMC) in 25 Chinese patients with ulcerative colitis and 20 healthy controls. METHODS: PBMC were isolated by density gradient centrifugation of heparinized blood and cultures for 24 or 48 hours by stimulation with LPS or PHA. TNF-alphaand sIL-2r were measured by ELISA method and IL-6 measured by biossay. RESULTS: TNF-alphaproduction stimulated by LPS and sIL-2r production by PHA in ulcerative colitis were significantly lower than in healthy controls (TNF-alpha509(46-7244)ng/L vs 1995(117-18 950)ng/L, P < 0.05; sIL-2r 320U/mlplus minus 165U/ml vs 451U/mlplus minus 247U/ml, P < 0.05).Spontaneous TNF-alphaand sIL-2r production were not significantly different between ulcerative colitis and controls (TNF-alpha304(46-7044)ng/L vs 215(46-4009)ng/L,P > 0.05; sIL-2r 264U/mlplus minus 115U/ml vs 236U/mlplus minus139U/ml, P>0.05). IL-6 production by spontaneous release from PBMC in ulcerative colitis group was 109U/mlplus minus 94U/ml vs 44U/mlplus minus 39U/ml for those in healthy controls, P < 0.01. IL-6 stimulated by LPS in ulcerative colitis group was (261U/ml plus minus 80U/ml) higher than in healthy controls (102U/mlplus minus 54U/ml, P < 0.01). No correlation of TNF-alpha, IL-6, sIL-2r production was found to disease activity, disease location and medication. CONCLUSION: Cytokine production from PBMC was also disturbed in Chinese patients with ulcerative colitis.
Authors: G Bouma; M Oudkerk Pool; J G Scharenberg; J J Kolkman; B M von Blomberg; R J Scheper; S G Meuwissen; A S Peña Journal: Scand J Gastroenterol Date: 1995-11 Impact factor: 2.423
Authors: S C Jones; L K Trejdosiewicz; R E Banks; P D Howdle; A T Axon; M F Dixon; J T Whicher Journal: J Clin Pathol Date: 1993-12 Impact factor: 3.411