[Immunopathogenetic and ultrastructural aspects of ulcerative colitis].

The ultrastructural pathology and local immune response in ulcerative colitis are discussed. The local immune reaction in ulcerative colitis is characterized by distinct plasma cell multiplication with a striking deviation from the normal mucosal immunocyte class pattern resulting in a disproportionate increase of the IgG-cell number. The pronounced local IgG-cell response in the bowel mucosa of patients with ulcerative colitis should probably be regarded as an attempt to establish a "second line of defense" against exogenous and/or endogenous antigens. In cases with active disease IgG is found to be bound to the basement membrane of the surface epithelium. Activated complement (Clq and C3 fraction) can be demonstrated at this site as well. This association of IgG and activated complement at the same site in the mucosa suggests the possible involvement of fixed immune complexes in the production of mucosal damage. The immune complexes presumably bound to the epithelial basement membrane and the consequent activation of complement could explain the marked granulocytic activities at the surface epithelium in active ulcerative colitis. These polymorphonuclear leukocytes could have been attracted by components of the activated complement. Granulocytes are often seen in state of degranulation. The degranulation of granulocytes (and macrophages) may be result of "frustrated phagocytosis" by the granulocytes and macrophages of antigen-antibody complexes. This process could induce the release of lysosomal enzymes by granulocytes and macrophages. The detection of extracellular lysosomal enzymes (peroxidase, acid phosphatase) could be of pathogenetic significance in connection with the concept of Weissmann. Lysosomal enzymes damage cells, connective tissue and mucosal block. This implies exacerbation and perpetuation of the antigenic breach and therefore of the inflammatory process. A vicious circle is started.