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(Journal of Leukocyte Biology. 2001;70:873-880.)
© 2001 by Society for Leukocyte Biology

Induction of syngeneic graft-versus-host disease in LPS hyporesponsive C3H/HeJ mice

Diana Lowery Flanagan*, Rachel Gross{dagger}, C. Darrell Jennings{ddagger}, Betty E. Caywood{dagger}, Sarah Goes*, Alan M. Kaplan* and J. Scott Bryson*,{dagger}

Departments of
* Microbiology and Immunology and
{ddagger} Pathology, and
{dagger} Blood and Marrow Transplant Program, Division of Hematology/Oncology, Department of Internal Medicine, Markey Cancer Center, University of Kentucky, Lexington

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

Syngeneic GVHD (SGVHD) develops following syngeneic bone marrow transplantation and treatment with cyclosporine A. Previous studies have demonstrated a role for IL-12, IFN-{gamma}, and TNF-{alpha} in the development of murine SGVHD. Macrophages can be activated to secrete IL-12 and TNF-{alpha} via a T-cell-dependent or T-cell-independent pathway (LPS or bacterial products). Studies were designed to determine if LPS participated in the development of SGVHD in C3H/HeN (LPS-responsive) and C3H/HeJ (LPS-hyporesponsive) mice. C3H/HeJ and C3H/HeN mice had similar levels of disease induction and pathology. Following induction of SGVHD, treatment of C3H/HeN, but not C3H/HeJ, mice with a sublethal dose of LPS resulted in mortality. However, neutralization of IL-12 abrogated the development of disease in C3H/HeJ mice, demonstrating that activated macrophages and their products participated in the development of SGVHD in these animals. These data suggested that LPS responsiveness was not a predisposing factor for SGVHD induction.

Key Words: bone marrow transplantation • cyclosporine A • lipopolysaccharide




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