Immunohistochemical changes in morphologically involved and uninvolved colonic mucosa of patients with idiopathic proctitis.

Isolation and characterization of colonic tissue-bound antibodies from patients with idiopathic ulcerative colitis

“…Table 1 shows binding of 125I-labeled CCA and 125I-labeled human IgG by diseased tissues obtained from six patients with ulcerative colitis and three patients with idiopathic proctitis, and the tissues (both diseased and normal) from eight control subjects, including two patients with Crohn disease, two patients with nonspecific diarrhea, one patient with bacillary dysentery, and three normal individuals. The binding of 125I-labeled CCA was significantly higher than the binding of '25I-labeled human IgG (12,20,21). Specificity for CCA is indicated by its ability to recognize colonic tissue from patients with ulcerative colitis and its lack of reactivity with diseased colonic tissue in Crohn disease, bacillary dysentery, and nonspecific diarrhea.…”

“…The colon eluate was tested by Ouchterlony immunodiffusion and immunoelectrophoresis with antisera against K and X light chains; Fab and Fc fragments of human IgG, y, A, and a chains; free secretory component; human IgE; albumin; fC; and C1q. The antisera against human immunoglobulin were obtained from Cappel Laboratory, Downington, PA. Antiserum to human free secretory component was prepared by us (12). Monospecificity of all the antisera was demonstrated by immunoelectrophoresis.…”

“…Circulating immune complexes and activated monocytes have been found in the blood of patients with active ulcerative colitis (10)(11). Recent studies have further demonstrated a deficient mucosal secretory IgA system which may compromise the mucosal defenses of the host (12)(13)(14). This study reports isolation of disease-specific antibody bound to colonic mucosa in patients with ulcerative colitis.…”

Immunological Mechanisms of Chronic Ulcerative Colitis

“…In testinal mononuclear cells front patients with IBD show in cultures depressed antibody production [89], On the other hand, others reported a normal proliferative response to mitogens [88]. The normal-appearing colonic mucosa proximal to the demarcation of CUC was found to be deficient in secretory IgA [90], This deficiency may be a primary immunodefect or perhaps the result of a prosta glandin-dependent suppressor system which inhibits IgA production after nonspecific stimulation [91]. Both findings have not been confirmed.…”

“…Both findings have not been confirmed. Others have found in the gut mu cosa an inverse relationship between the staining of s-IgA and the degree of inflamma tion and dysplasia, reflecting more likely sec ondary phenomena [92], Earlier reports on decreased secretory components of salivary IgA in patients with CUC [95] have been questioned [90,94], Cytotoxicity of gut lymphocytes of pa tients with CUC for autologous or allogeneic colon epithelial cells has not been docu mented. Experiments demonstrating the role of gut lymphocytes in mediating ADCC or in natural killer cell activity for other target cells are not clear cut [ 1,85,96,97] due to techni cal artifacts and methodological differences [85,98].…”