Cutting Edge: HMG-1 as a Mediator of Acute Lung Inflammation

Journal of Immunology - Tập 165 Số 6 - Trang 2950-2954 - 2000
Edward Abraham1, John J. Arcaroli1, Aaron B. Carmody1, Haichao Wang2, Kevin J. Tracey2
1*Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, CO 80262; and
2†Laboratory of Biomedical Science, North Shore University Hospital-New York University School of Medicine, Manhasset, NY 11030

Tóm tắt

Abstract 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-1β, TNF-α, 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-1β, TNF-α, 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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Journal of Immunology

Tập 165 Số 6

2950-2954

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