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(Journal of Leukocyte Biology. 2002;72:762-768.)
© 2002 by Society for Leukocyte Biology

Nitric oxide participates in the intestinal pathology associated with murine syngeneic graft-versus-host disease

D. M. Flanagan^*,, C. D. Jennings, S. W. Goes, B. E. Caywood, R. Gross, A. M. Kaplan and J. S. Bryson^,

^* Department of Biology, Hardin-Simmons University, Abilene, Texas; and Departments of
Microbiology, Immunology and Molecular Genetics,
Pathology, and
Internal Medicine, Markey Cancer Center, Chandler Medical Center, University of Kentucky, Lexington

Correspondence: J. Scott Bryson, Ph.D., Associate Professor, Blood and Marrow Transplant Program, Division of Hematology Oncology, Department of Internal Medicine, Markey Cancer Center, University of Kentucky, Lexington, KY 40536-0093. E-mail: jsbrys{at}uky.edu

Syngeneic graft-versus-host disease (SGVHD) develops following lethal irradiation, reconstitution with syngeneic bone marrow, and treatment with a short course of cyclosporin A (CsA) therapy. The disease is characterized by the development of a T helper cell type 1-like cytokine response [interleukin (IL)-12, interferon- (IFN-), and tumor necrosis factor ], and macrophage activation is central to development of the syndrome. It has been shown that nitric oxide (NO) participates significantly in the development of allogeneic GVHD. Studies were initiated to determine if NO participates in the pathology associated with SGVHD. Significant increases in inducible NO synthase (iNOS) mRNA and circulating NO were found in the tissues of SGVHD versus control animals. Treatment of SGVHD animals with the iNOS inhibitor aminoguanidine (AG) reversed the pathology associated with this disease. Furthermore, AG treatment reduced the production of IL-12 and IFN- mRNA in the colons of CsA-treated mice. These studies demonstrate that NO participates in the pathological processes that are associated with the development of murine SGVHD.

Key Words: IFN- • interleukin-12 • nitric oxide • aminoguanidine

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