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Blood, Vol. 93 No. 11 (June 1), 1999:
pp. 4006-4010
Red Blood Cells Inhibit Apoptosis of Human Neutrophils
Kazutetsu Aoshiba,
Yuri Nakajima,
Shuji Yasui,
Jun Tamaoki, and
Atsushi Nagai
From First Department of Medicine, Tokyo Women's Medical University,
8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan.
Oxidative stress has been implicated in the triggering of apoptosis
in neutrophils. Because red blood cells (RBCs) are well known to
scavenge oxidants including H2O2, we tested the
hypothesis that RBCs inhibit apoptosis of neutrophils by reducing
intracellular oxidative stress. Apoptosis of neutrophils was evaluated
by light microscopy and DNA gel electrophoresis. We found that
coculture with RBCs protected against neutrophil apoptosis. Neither
physical contact between RBCs and neutrophils nor the cellular
integrity of RBCs was required to protect against neutrophil apoptosis. Neutrophil apoptosis was promoted by exogenous
H2O2 but suppressed by catalase, indicating a
role for H2O2 as a mediator of apoptosis. The
protective effect of RBCs against apoptosis was due to catalase and
glutathione metabolism because blocking of these antioxidant systems in
RBCs attenuated the protective effect of RBCs. These results suggest
that neutrophils are protected against apoptosis in the circulation.
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