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CUTTING EDGE |
*
Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, CO 80262; and
Laboratory of Biomedical Science, North Shore University Hospital-New York University School of Medicine, Manhasset, NY 11030
Acute inflammatory lung injury is often a delayed complication
of critical illness and is associated with increased mortality. High
mobility group-1 (HMG-1) protein, in addition to its role as a
transcriptional regulatory factor, has recently been identified as a
late mediator of endotoxin lethality. In the present studies, HMG-1
given intratracheally produced acute inflammatory injury to the lungs,
with neutrophil accumulation, the development of lung edema, and
increased pulmonary production of IL-1ß, TNF-
, and
macrophage-inflammatory protein-2. In endotoxin-induced acute lung
inflammation, administration of anti-HMG-1 Abs either before or
after endotoxin exposure decreased the migration of neutrophils to the
lungs as well as lung edema. These protective effects of anti-HMG-1
were specific, because pulmonary levels of IL-1ß, TNF-, or
macrophage-inflammatory protein-2 were not decreased after therapy with
anti-HMG-1. Together, these findings indicate that HMG-1 is a
distal mediator of acute inflammatory lung
injury.
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