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Departments of
*
Medicine and
Pediatrics, and
Program in Molecular Signal Transduction, National Jewish Medical and Research Center, Denver, CO 80206; and
§
Division of Pulmonary Science and Critical Care Medicine, University of Colorado School of Medicine, Denver, CO 80262
Early inflammatory events include cytokine release, activation, and
rapid accumulation of neutrophils, with subsequent recruitment of
mononuclear cells. The p38 mitogen-activated protein kinase (MAPK)
intracellular signaling pathway plays a central role in regulating a
wide range of inflammatory responses in many different cells. A murine
model of mild LPS-induced lung inflammation was developed to
investigate the role of the p38 MAPK pathway in the initiation of
pulmonary inflammation. A novel p38 MAPK inhibitor, M39, was used to
determine the functional consequences of p38 MAPK activation. In vitro
exposure to M39 inhibited p38 MAPK activity in LPS-stimulated murine
and human neutrophils and macrophages, blocked TNF-
and macrophage
inflammatory protein-2 (MIP-2) release, and eliminated migration of
murine neutrophils toward the chemokines MIP-2 and KC. In contrast,
alveolar macrophages required a 1000-fold greater concentration of M39
to block release of TNF- and MIP-2. Systemic inhibition of p38 MAPK
resulted in significant decreases in the release of TNF- and
neutrophil accumulation in the airspaces following intratracheal
administration of LPS. Recovery of MIP-2 and KC from the airspaces was
not affected by inhibition of p38 MAPK, and accumulation of mononuclear
cells was not significantly reduced. When KC was instilled as a
proinflammatory stimulus, neutrophil accumulation was significantly
decreased by p38 MAPK inhibition independent of TNF- or LPS.
Together, these results demonstrate a much greater dependence on the
p38 MAPK cascade in the neutrophil when compared with other leukocytes,
and suggest a means of selectively studying and potentially modulating
early inflammation in the lung.
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M. J. Rane, P. Y. Coxon, D. W. Powell, R. Webster, J. B. Klein, W. Pierce, P. Ping, and K. R. McLeish p |
