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*
Departments of Surgery, The Toronto Hospital and University of Toronto, Toronto, Ontario, Canada;
Defense and Civil Institute of Environmental Medicine, Toronto, Ontario, Canada; and
National Institutes of Health-National Institute of Dental Research, Bethesda, MD 20892
Recent studies have suggested that hemorrhagic shock followed by
resuscitation renders patients more susceptible to lung injury by
priming for an exaggerated response to a second stimulus, the so-called
"two-hit" hypothesis. We investigated the role of C-X-C chemokines
in mediating the augmented lung inflammation in response to LPS
following resuscitated shock. In a rodent model, animals exposed to
antecedent shock exhibited enhanced lung neutrophil sequestration and
transpulmonary albumin flux in response to intratracheal LPS. This
effect correlated with an exaggerated expression of cytokine-induced
neutrophil chemoattractant (CINC) protein and mRNA, but not
macrophage-inflammatory protein 2. Strategies designed to inhibit CINC,
both anti-CINC Ab and supplementation with the antioxidant
N-acetyl-cysteine, prevented the enhanced neutrophil
sequestration, suggesting that CINC played a central role in the
enhanced leukocyte accumulation following shock plus LPS treatment.
Shock alone increased lung nuclear factor-
B expression and augmented
the response to LPS. Prevention of this effect by
N-acetyl-cysteine supplementation of the resuscitation
fluid implicates a role for oxidant stress in the priming for lung
inflammation following shock. Finally, alveolar macrophages recovered
from shock-resuscitated animals released more CINC protein in vitro in
response to LPS than macrophages from sham animals. Considered
together, these findings show that augmented release of CINC, in part
from primed alveolar macrophages, contributes significantly to the
enhanced lung leukosequestration and transpulmonary albumin flux in
response to LPS following resuscitated shock.
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