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From the Department of Trauma Surgery,*
University of
Freiburg Medical School, Freiburg/Breisgau, Germany, and the Department
of Pathology,
University of Michigan Medical
School, Ann Arbor, Michigan
A major complication in sepsis is progressively impaired lung
function and susceptibility to intrapulmonary infection. Why sepsis
predisposes the lung to injury is not clear. In the current
studies, rats were rendered septic by cecal ligation/puncture
and evaluated for increased susceptibility to injury after a direct
pulmonary insult (deposition of IgG immune complexes or airway
instillation of lipopolysaccharide). By itself, cecal
ligation/puncture did not produce evidence of lung injury.
However, after a direct pulmonary insult, lung injury
in septic animals was significantly enhanced. Enhanced lung injury was
associated with increased accumulation of neutrophils in lung,
enhanced production of CXC chemokines (but not tumor necrosis
factor-
) in bronchoalveolar lavage fluids, and increased
expression of lung vascular intercellular adhesion molecule-1 (ICAM-1).
Complement depletion or treatment with anti-C5a abolished all evidence
of enhanced lung injury in septic animals. When stimulated in
vitro, bronchoalveolar lavage macrophages from septic
animals had greatly enhanced CXC chemokine responses as compared with
macrophages from sham-operated animals or from septic animals that had
been complement depleted. These data indicate that the septic state
causes priming of lung macrophages and suggest that enhanced lung
injury in the septic state is complement dependent and related to
increased production of CXC chemokines.
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