Histopathology of cell mediated immune reaction in mouse colon--allograft rejection.

Abstract

SUMmARY Grafts of mouse fetal colon, implanted beneath the renal capsule of adult hosts, have been used to study the growth and development of colonic isografts and the rejection of colonic allografts. Isografts grew normally and maintained a structure similar to normal colon. Grafts between strains with H2 histocompatibility differences were rejected by 13 days after transplantation. Early progressive infiltration of the grafts by lymphoid cells was followed by increasing damage to, and subsequent loss of, the epithelial cell layer and destruction of the underlying muscle, changes which parallel those seen in rejection of skin and small bowel. The increase in survival time which is seen in allografts between strains with H2 identity was longer in the colon than has been seen in the skin or small bowel; none of the allografts of colon were completely rejected before 30 days, and some remained viable at 50 days. Comparison of the appearances of rejection in the colon withthose of ulcerative colitis and colonic Crohn's disease does not show the striking similarity which is seen between small bowel rejection and coeliac disease. Many of the individual features of these diseases are, however, present in the course of colonic rejection.

Effects of age, antigen deprivation, and allograft rejection on epithelial cell kinetics in mouse colon.

“…Allografts and isografts grew satisfactorily, as described in previous reports (Ferguson and Parrott, 1972;Holden and Ferguson 1976;MacDonald and Ferguson, 1977). Isografts grew progressively larger after implantation; allografts grew for seven to 10 days before rejection.…”

“…The method is applicable to normal colon of animals at any age and its application to grafts of foetal mouse colon has allowed definition of the effects of several factors on cell kinetics. The experimental situations examined here-of normal post-natal growth, of antigen-free growth in isografts, and the effects of cell-mediated immunity-parallel those examined in a previous morphological study (Holden and Ferguson 1976 (Dowling et al, 1967;Stragand and Hagemann, 1977). Alternatively, immune reactions between mucosal lymphoid tissues and antigens present in food or bacteria in the bowel lumen may be the initiating factor causing the rise in cell turnover.…”

“…There was lymphocyte infiltration but with a reduction in the number of mucous cells and with shortening of the crypts as compared with crypts of isografts of similar age (Holden and Ferguson, 1976). However, the cell kinetic studies have now shown that the short allograft crypts have a two-to three-fold greater rate of cell production than occurs in isografts or normal intestine of the same age.…”

“…In the small intestine and colon, the proliferative region is in the lower part of the crypt and the cells migrate upwards towards the surface as they mature (Lipkin, 1973). In a previous report (Holden and Ferguson, 1976), we described the morphological development of normal mouse colon, and the effects of an antigenfree state (isografts of mouse colon) and local cellmediated immune damage (rejection of colonic allografts) on morphology. The effects of a local cell-mediated immune reaction on the colon were contrasted with those of similarly induced damage to the small intestine.…”

Transfer of Colon Inflammatory Disease from Immune to Normal Guinea Pigs by Lymphocytes

“…The histology of the colon of both lym phocyte donors and recipients showed fea tures previously reported to be associated with cell mediated immune rejection of colon allografts in mice [6,7], This similarity supports the role of cell-mediated immune mechanisms in the pathogenesis of the his tologic alterations observed with adoptive lymphocyte transfer.…”