CYTOKINE PRODUCTION IN THE MUCOSA OF PATIENTS WITH INFLAMMATORY BOWEL-DISEASE

被引:10
作者
JONES, SC
HAIDAR, A
HAGAN, P
CRABTREE, JE
BANKS, RE
AXON, ATR
DIXON, MF
WHICHER, JT
机构
[1] Centre for Digestive Diseases, Leeds General Infirmary, Leeds
[2] Department of Endocrinology, National Institute for Biological Standards and Controls, Potters Barr, Hertfordshire
[3] Department of Clinical Medicine, St James’s University Hospital, Leeds
[4] Institute for Cancer Studies, St James’s University Hospital, Leeds
关键词
INTERLEUKIN-6; TUMOR NECROSIS FACTOR; INFLAMMATORY BOWEL DISEASE;
D O I
10.1097/00042737-199308000-00009
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Objective: To investigate mucosal secretion of interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) in inflammatory bowel disease patients and controls. Design: Prospective study of patients recruited from the colonoscopy lists and the colitis clinic of a teaching hospital gastroenterology unit. Methods: Mucosal biopsies from patients with inflammatory bowel disease and controls were cultured for 24 h and secretion of IL-6 and TNF-alpha was determined by enzyme-linked immunosorbent assay. Results: Interleukin-6 and TNF-alpha production in vitro from patients with active ulcerative colitis was significantly greater than from patients with inactive ulcerative colitis (P<0.005), inflamed mucosa in patients with Crohn's disease (P<0.05) and controls (P<0.005). Interleukin-6 production from inactive ulcerative colitis biopsy specimens was also significantly greater than from controls (P<0.02). Interleukin-6 and TNF-alpha secretion by ulcerative colitis biopsy specimens correlated with both acute and chronic inflammatory cell infiltrate (P < 0.002) and surface epithelial degeneration of the mucosa (P < 0.001). Conclusions: Interleukin-6 and TNF-alpha are secreted locally by the inflamed colonic mucosa in ulcerative colitis and Crohn's disease. The higher concentration of IL-6 in the supernatants from ulcerative colitis biopsy specimens contrasts with circulating IL-6 concentrations, which are higher in patients with Crohn's disease.
引用
收藏
页码:607 / 612
页数:6
相关论文
共 42 条
[1]  
Pober J.S., Bevilacqua M.P., Mendrick D.L., Lapierre L.A., Fiers W., Gimbrone M.A., Two distinct monokines, interleukin-l andtumour necrosis factor, each independently induce biosynthesis and transient expression of the same antigen on the surface of cultured human vascular endothelial cells, J Immunol, 136, pp. 1680-1687, (1986)
[2]  
Klebanoff S.J., Vadas M.A., Harlan J.S., Sparks L.H., Gamble J.R., Agosti J.M., Et al., Stimulation of neutrophils by tumour necrosis factor, J Immunol, 136, pp. 4220-4225, (1986)
[3]  
Tsujimoto M., Yokota S., Vilcek J., Weissman G., Tumour necrosis factor provokes superoxide anion generation from neutrophils, Biochem Biopbys Res Commun, 137, (1986)
[4]  
Nawroth P.P., Stern D.M., Modulation of endothelial cell haemostatic properties by tumour necrosis factor, J Exp Med, 163, pp. 740-745, (1986)
[5]  
Djeu J.Y., Blanchard D.K., Richards A.L., Freidman H., Tumour necrosis factor induction by Candida albicans from human natural killer cells and monocytes, J Immunol, 141, pp. 4047-4052, (1988)
[6]  
Kunkel S.L., Streiter R.M., Chensue S.W., Basha M., Standiford T., Ham J., Et al., Tumour necrosis factor-alpha, interleukin-8 and chemotactic cytokines, Prog Clin Biol Res, 349, pp. 433-444, (1990)
[7]  
Lotz M., Jirik F., Kabouridis R., Tsoukas C., Hirano T., Kishimoto T., Cell stimulating factor 2/interleukin-6 is a costimulant for human thymocytes and Τ lymphocytes, J Exp Med, 167, pp. 1253-1258, (1988)
[8]  
Hirano T., Taga T., Nakano N., Yasukawa K., Kashiwamura S., Shimizu K., Et al., Purification to homogeneity and characterization of human B-cell differentiation factor (BCDF or BSFp-2), Proc Natl Acad Sci USA, 82, pp. 5490-5494, (1985)
[9]  
Borish L., Rosenbaum R., Albury L., Clark S., Activation of neutrophils by recombinant interIeukin-6, Cell Immunol, 121, pp. 280-289, (1989)
[10]  
Salas M.A., Evans S.W., Levell M.J., Wwcher J.T., Interleukin-6 and ACTH act synergistically to stimulate the release of corticosterone from adrenal glands, Clin Exp Immunol, pp. 79470-79473, (1990)