[Activation of nuclear factor-kappaB and effects of anti-inflammatory treatment thereon in intestinal mucosa of patients with ulcerative colitis].

To investigate the activation and expression of nuclear factor-kappaB (NF-kappaB) and effects of anti-inflammatory treatment on NF-kappaB in the intestinal mucosa of patients with ulcerative colitis (UC). Ten pieces of colon mucosal biopsy specimens were obtained from 31 cases with UC, 17 of which received sulphasalazine (SASP) or SASP plus glucocorticoid and 14 of which received no medication. Samples of normal mucosa around the lesion taken from 11 patients with colon cancer were used as controls. NF-kappaB DNA binding activity was evaluated by electrophoretic mobility shift assay. NF-kappaB p65 expression was determined by Western blot analysis and immunohistochemical staining with a NF-kappaB p65 antibody. The type of cells containing activated NF-kappaBp65 was identified by double immunofluorescence confocal laser scanning microscopy. The expression of NF-kappaB p65 and NF-kappaB DNA binding activity were significantly higher in patients with UC than in the control (P < 0.05), and were correlated with the degree of inflammation. The NF-kappaB expression was significantly stronger in the nuclei than in the cytoplasm in patients with UC without pharmacotherapy. The NF-kappaB expression in nuclei was significantly stronger in the group without pharmacotherapy than in the group with pharmacotherapy (P < 0.05). Only a few NF-kappaB p65 positive cells were seen in the controls. NF-kappaBp65 expression was found in all major subsets of mononuclear cells, including macrophages, B lymphocytes, T lymphocytes, and cryptal epithelial cells. The increased activation of NF-kappaB and increased expression of NF-kappaB may be involved in the pathogenesis of UC. Glucocorticoids and SASP strongly inhibited NF-kappaB activation and expression. The inhibition of NF-kappaB activation may be a central part of the anti-inflammatory action of glucocorticoids and SASP, which might represent an important pharmacological mechanism in treatment of patients with UC. NF-kappaB will be an important target for cytokine-based therapy of UC.