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B and MAPK/ERK
mechanisms
1 Center for Surgical Research and Departments of Surgery and 2 Anesthesiology, University of Alabama at Birmingham, Birmingham, Alabama 35294
The acute respiratory distress
syndrome (ARDS) is a major cause of morbidity after injury. We
hypothesized that alveolar macrophage (AM
) chemokine and cytokine
release after hemorrhage and sepsis is regulated by NF-
B and MAPK.
Adult male rats underwent soft tissue trauma and hemorrhagic shock
(~90 min) followed by crystalloid resuscitation. Sepsis was induced
by cecal ligation and puncture (CLP) 20 h after
resuscitation. AM were harvested, and TNF-
, IL-6, and
macrophage inflammatory protein (MIP)-2 release and serum IL-6 and
TNF- levels were measured at 5 h after HCLP. Lung tissues were
analyzed for activation of NF-B, myeloperoxidase activity, and
wet/dry weight ratio. In control animals, AM were stimulated with
LPS with or without inhibitors of NF-B and MAPK. Serum TNF- and
IL-6 levels and spontaneous AM TNF- and MIP-2 release were
elevated (P < 0.05) after HCLP, concomitantly with the
development of lung edema and leukocyte activation. Activation of
NF-B increased in lungs from the hemorrhage and CLP group compared
with shams. Inhibition of NF-B or the upstream MAPK significantly
decreased LPS-stimulated AM activation. Because enhanced release of
inflammatory mediators by AM may contribute to ARDS after severe
trauma, inhibition of intracellular signaling pathways represents a
target to attenuate organ injury under those conditions.
mitogen-activated protein kinase; leukocytes; macrophage
inflammatory protein; acute respiratory distress syndrome; extracellular signal-regulated kinase; nuclear factor-B
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