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Aplastic anemia: analysis of stromal cell function in long-term marrow
cultures
LA Holmberg, K Seidel, W Leisenring and B Torok-Storb
Fred Hutchinson Cancer Research Center, Seattle, WA 98104.
Marrow samples from 89 patients with aplastic anemia (AA) were evaluated
for their ability to grow stromal layers in standard long- term marrow
cultures (LTMCs). Results were highly variable: 6.8% failed to grow any
stromal cells (group I); 42.5% either failed to grow to confluency or
appeared to have a decreased number of adipocytes and/or macrophages (group
II); and 52.8% appeared as normal confluent cultures with fibroblasts,
adipocytes, and macrophages (group III). Analyses of patient data suggested
that group I patients had a longer disease duration and poorer survival (P
= .07). Enzyme-linked immunosorbent assay analysis of cytokine production
was performed on 20 of the normal- appearing AA LTMCs and 12 LTMCs
established from normal donors. Significant differences between the AA and
control groups were apparent for macrophage inflammatory protein-1 alpha
(MIP-1 alpha), interleukin- 1 receptor antagonist (IL-1ra),
granulocyte-macrophage colony- stimulating factor (GM-CSF), granulocyte
colony-stimulating factor (G- CSF), and leukemia-inhibitory factor (LIF).
The most dramatic differences observed were elevated levels of MIP-1 alpha
and GM-CSF and decreased levels of IL-1ra, particularly after IL-1 alpha
stimulation. In contrast, IL-1 alpha stimulation of AA LTMCs produced
levels of IL- 6, LIF, and G-CSF comparable with those of controls. These
data suggest that defects exist within the microenvironment of some AA
marrows. Whether the majority of these defects are the cause or consequence
of aplasia is not clear. However, we speculate that some of these
abnormalities may contribute to the maintenance of the hypoplastic state
and, in extreme cases, prevent engraftment of donor marrow.
Volume 84,
Issue 11,
pp. 3685-3690,
12/01/1994
Copyright © 1994 by The American Society of Hematology
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