Peanut lectin binding sites in colons of patients with ulcerative colitis.

We studied peanut lectin (PNA) binding sites in patients with ulcerative colitis (UC) with various degrees of disease activity and dysplasia. Peanut lectin binds to B-D-galactose (1-3) N-acetyl-D-galactosamine, which is the purported determinant for the T-blood-group antigen and the immediate precursor of the MN-blood-group glycoprotein. In the normal colon, PNA binds to the supranuclear (SN) portion of goblet and columnar cells, representing nascent glycoproteins in the Golgi apparatus prior to the addition of terminal sialic acid. In severely active UC, PNA binds to the glycocalyx and/or apical portion of columnar cells, crypt goblet cells, and the total cytoplasm of "regenerating or hyperplastic" epithelium. These patterns have been previously reported in colonic cancers, adenomas, and fetal colons, indicating the synthesis of incomplete glycoproteins. Cases of inactive UC and mildly active UC expressed PNA binding in an SN distribution similar to controls. Cases with dysplasia showed PNA binding patterns similar to colonic neoplasms. In UC, the perturbation of cell kinetics similar to colonic neoplasms and the more rapid cell migration and turnover may be reflected as synthesis of incomplete glycoproteins, as expressed by abnormal PNA binding patterns. These findings indicate that the epithelial cells in patients with severely active UC synthesize incomplete glycoproteins similar to colonic neoplasms; however, this abnormal glycoprotein pattern is reversible when inflammation is more quiescent.