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Blood, Vol. 92 No. 10 (November 15), 1998:
pp. 3960-3967
Keratinocyte Growth Factor Administered Before Conditioning
Ameliorates Graft-Versus-Host Disease After Allogeneic Bone Marrow
Transplantation in Mice
Angela Panoskaltsis-Mortari,
David L. Lacey,
Daniel A. Vallera, and
Bruce R. Blazar
From the University of Minnesota Cancer Center and Department of
Pediatrics, Division of Bone Marrow Transplantation, and Department of
Therapeutic Radiology-Radiation Oncology, University of Minnesota,
Minneapolis, MN; and Amgen Inc, Thousand Oaks, CA.
Keratinocyte growth factor (KGF) is important in tissue repair and
wound healing and its administration can abrogate chemical- and
radiation-induced tissue damage in rodents. We investigated KGF as a
therapeutic agent for the prevention of graft-versus-host disease
(GVHD)-induced tissue damage, morbidity, and mortality in an
established murine allogeneic bone marrow transplantation (BMT) model.
B10.BR (H2k) recipient mice were lethally irradiated and
transplanted with C57BL/6 (H2b) bone marrow (BM) with
spleen cells (BMS) as a source of GVHD-causing T cells. KGF-treated
mice (5 mg/kg/d subcutaneously days  6, 5, and 4 pre-BMT)
receiving BMS exhibited better survival than those not receiving KGF
(P = .0027). Cyclophosphamide (Cy), a common component of
total body irradiation (TBI)-containing regimens, was administered to
other cohorts of mice at a dose of 120 mg/kg/d intraperitoneally on
days 3 and 2 before BMT. KGF-treated mice again exhibited a
better survival rate than those not receiving KGF (P = .00086). However, KGF-treated recipients receiving TBI or Cy/TBI BMS
were not GVHD-free, as shown by lower body weights compared with BM
groups. GVHD target tissues were assessed histologically during a
38-day post-BMT observation period. KGF ameliorated GVHD-induced tissue
damage in the liver, skin, and lung (completely in some recipients) and
moderately so in the spleen, colon, and ileum, even with Cy
conditioning. These studies demonstrate that KGF administration,
completed before conditioning, has potential as an anti-GVHD
therapeutic agent.
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