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,
*
Division of Pulmonary and Critical Care Medicine, and
Division of Rheumatology, Department of Medicine, New York University Medical Center, New York, NY 10016; and
Department of Rheumatology, Hospital for Joint Diseases, New York, NY 10003
GM-CSF has a major role in the immune and inflammatory milieu of
the airway. Airway epithelial cells (AEC) are among the first targets
of environmental stimuli and local cytokines, in response to which they
can produce GM-CSF. The regulation of GM-CSF is only minimally
understood in AEC. We hypothesized that GM-CSF expression in AEC would
result from activation of protein kinase C (PKC) and subsequent
activation of the extracellular signal-regulated kinase
(MAPKerk1/2) pathway, so we investigated signal
transduction pathways in human primary culture bronchial epithelial
cells (HBECs). TNF-
, IL-1ß, and PMA induced the release of GM-CSF
in HBECs. The robust response to PMA was not detected in SV40
adenovirus-transformed normal human bronchial epithelial cells
(BEAS-2B). PMA and TNF- stimulation of GM-CSF required activation of
PKC (inhibition by staurosporine and bisindolylmaleimide I). GM-CSF
expression was up-regulated by a nonphorbol PKC activator, but not by
an inactive PMA analogue. PMA-induced GM-CSF production in HBECs did
not require a Ca2+ ionophore and was not inhibited by
cyclosporin A. Activation of MAPKerk1/2 via PKC was
associated with and was required for GM-CSF production induced by PMA
and TNF-. The data demonstrate regulation of GM-CSF in HBECs by PKC
pathways converging on the MAPKerk1/2 pathway and further
define cell-specific regulation critical for local airway
responses.
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