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B, and Cyclic Adenosine 5'-Monophosphate Response Element-Binding Protein in Lung Neutrophils Occurs by Differing Mechanisms After Hemorrhage or Endotoxemia1
Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Science Center, Denver, CO 80262
Acute lung injury is frequently associated with sepsis or blood
loss and is characterized by a proinflammatory response and
infiltration of activated neutrophils into the lungs. Hemorrhage or
endotoxemia result in activation of cAMP response element-binding
protein (CREB) and NF-
B in lung neutrophils as well as increased
expression of proinflammatory cytokines, such as TNF-
and
macrophage-inflammatory peptide-2, by these cells. Activation of the
extracellular regulated kinase (ERK) pathway occurs in stress responses
and is involved in CREB activation. In the present experiments,
hemorrhage or endotoxemia produced increased activation of
mitogen-activated protein kinase kinase (MEK)1/2 and ERK2 (p42), but
not of ERK1 (p44), in lung neutrophils. ERK1, ERK2, and MEK1/2 were not
activated in peripheral blood neutrophils after hemorrhage or
endotoxemia. Inhibition of xanthine oxidase led to further increase in
the activation of MEK1/2 and ERK2 in lung neutrophils after hemorrhage,
but not after endotoxemia. -Adrenergic blockade before hemorrhage
resulted in increased activation in lung neutrophils of MEK1/2, ERK1,
ERK2, and CREB, but decreased activation of NF-B. In contrast,
-adrenergic blockade before endotoxemia was associated with
decreased activation of MEK1/2, ERK2, and CREB, but increased
activation of NF-B. 
-Adrenergic blockade before hemorrhage did
not alter MEK1/2 or ERK1 activation in lung neutrophils, but decreased
activation of ERK2 and CREB, while increasing activation of NF-B.
-Adrenergic inhibition before endotoxemia did not affect activation
of MEK1/2, ERK1, ERK2, CREB, or NF-B. These data indicate that the
pathways leading to lung neutrophil activation after hemorrhage are
different from those induced by endotoxemia.
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