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Reduction of murine Syngeneic graft‐versus‐host disease (SGVHD) following treatment with the superoxide dismutase mimetic MnTBAP

Syngeneic graft‐vs‐host disease (SGVHD) is induced by reconstituting lethally irradiated mice with syngeneic bone marrow followed by a 21 day treatment with the immunosuppressive agent cyclosporine A (CsA). Symptoms of the disease appear 2–3 weeks following cessation of CsA therapy and disease‐associated inflammation occurs primarily in the colon and liver. Irradiation and CsA are both required for the development of SGVHD and both contribute to the production of oxidative stress. Time course studies revealed increased reactive oxygen and nitrogen species in CsA treated animals compared to BMT controls. Studies also demonstrated increased migration of CD4+T cells into the colon during CsA therapy. In addition, increased colon mRNA levels of proinflammatory cytokines (TNF‐α, IL‐12) and cell adhesion molecules (CAMs) were observed as early as day 14‐post BMT in colon of CsA treated animals. Since reactive oxygen species (ROS) are known to mediate CsA toxicity, studies were undertaken to determine the effect of CsA‐induced oxidative stress on the induction of SGVHD. Treatment with the antioxidant MnTBAP, during CsA therapy, caused a reduction in SGVHD development as well as decreased colon mRNA levels for iNOS, CAMs and proinflammatory cytokines. These studies suggest a role for oxidative stress in the development of intestinal pathology associated with murine SGVHD. Research support: NIH Grant P01‐CA092372.