Journal
JOURNAL OF IMMUNOLOGY
Volume 165, Issue 6, Pages 2950-2954Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.165.6.2950
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Funding
- NHLBI NIH HHS [HL50284, HL62221] Funding Source: Medline
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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-I given intratracheally produced acute inflammatory Injury to the lungs, with neutrophil accumulation, the development of lung edema, and increased pulmonary production of IL-1 beta, TNF-alpha, and macrophage-inflammatory protein-2, In endotoxin-induced acute lung inflammation, administration of anti-HMG-l 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-1 beta, TNF-alpha, or macrophage-inflammatory protein-2 were not decreased after therapy with anti-HMG-l, Together, these findings indicate that HMG-1 is a distal mediator of acute inflammatory lung injury.
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