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B Regulation in Human Neutrophils by Nuclear IB
: Correlation to Apoptosis1
Division of Neonatal-Perinatal Medicine, Schneider Children’s Hospital, Long Island Jewish Medical Center-The Long Island Campus, Albert Einstein College of Medicine, and North Shore-Long Island Jewish Research Institute, New Hyde Park, NY 11040
Neutrophils are among the first circulating leukocytes involved in
acute inflammatory processes. Transcription factor NF-
B plays a key
role in the inflammatory response, regulating the expression of
proinflammatory and anti-apoptotic genes. Recently we have shown
that human neutrophils contain a significant amount of NF-B
inhibitor, IB
, in the nucleus of unstimulated cells. The present
objective was to examine the mechanisms controlling the nuclear content
of IB in human neutrophils and to determine whether increased
accumulation of IB in the nucleus is associated with increased
neutrophil apoptosis. We show for the first time that neutrophil
stimulation with pro-inflammatory signals results in degradation of
IB that occurs in both cytoplasm and nucleus. Prolonged (2-h)
stimulation with TNF and LPS induces resynthesis of IB that is
again translocated to the nucleus in human neutrophils, but not in
monocytic cells. Leptomycin B, a specific inhibitor of nuclear export,
increases nuclear accumulation of IB in stimulated neutrophils by
blocking the IB nuclear export, and this is associated with
inhibition of NF-B activity, induction of caspase-3 activation, and
apoptosis. Based on our data we present a new model of NF-B
regulation in human neutrophils by nuclear IB. Our results
demonstrate that the NF-B activity in human neutrophils is regulated
by mechanisms clearly different from those in monocytes and other human
cells and suggest that the increased nuclear content of IB in
human neutrophils might represent one of the underlying mechanisms for
the increased apoptosis in these cells.
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