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1 Institute for Nutrition Research, University of Oslo; 2 Institute for Experimental Medical Research, and 3 Department of Cardiothoracic Surgery, Ullevål University Hospital, 0316 Oslo, Norway
Patients with heart failure are predisposed
to infections and anemia, possibly due to reduced hematopoiesis. The
proinflammatory cytokine tumor necrosis factor-
(TNF-) is
increased in heart failure, and it inhibits normal hematopoiesis,
partly due to apoptosis through the effector molecule Fas. We
examined bone marrow progenitor cells of mice with heart failure
induced by acute myocardial infarction. The fraction of progenitor
cells in mice with heart failure was only ~40% of control. Measured
with in vitro clonal assays, the proliferative capacity of the
progenitor cells in mice with heart failure was reduced to ~50% of
control. Flow cytometry with specific markers revealed a threefold
increase in apoptosis among progenitor cells from mice with
heart failure. In these mice, TNF-/Fas expression was increased in
bone marrow natural killer (NK) and T cells, and these
lymphocytes showed increased cytolytic activity in vitro against
progenitor cells. We conclude that the TNF-/Fas pathway in
lymphocytes is activated in the bone marrow during heart failure, which
may play a pathogenic role in the observed decrease in hematopoiesis.
blood cells; bone marrow cells; immunity; myocardial infarction
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