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Chemokines in Lung Injury*: Thomas A. Neff Lecture

Robert M. Strieter, MD, FCCP; Steven L. Kunkel, MD; Michael P. Keane, MBBCh; Theodore J. Standiford, MD
Author and Funding Information

*From the Departments of Internal Medicine (Drs. Strieter, Keane, and Standiford) and Pathology (Dr. Kunkel), Division of Pulmonary and Critical Care Medicine, The University of Michigan Medical School, Ann Arbor, MI.

Correspondence to: Robert M. Strieter, MD, FCCP, Department of Internal Medicine, Division of Pulmonary and Critical Care, University of Michigan Medical Center, 6200 MSRB III, 1150 W Medical Center Dr, Ann Arbor, MI 48109-0642; e-mail: rstriete@umich.edu



Chest. 1999;116(suppl_1):103S-110S. doi:10.1378/chest.116.suppl_1.103S
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Extract

Acute lung injury is due to a variety of direct or indirect insults leading to pulmonary inflammation. Several clinical entities, including trauma, pneumonia/sepsis, and ischemia-reperfusion injury are characterized by varying degrees of pulmonary insult that result in functional impairment of gas transfer in the lung. These events lead to an inflammatory response that is characterized by the following: recognition of the site of injury by inflammatory cells; specific recruitment of subpopulations of leukocytes into tissue; removal of the offending agent and “debridement” of the injured cells/tissue; and repair of the site of injury with attempts to reestablish normal parenchymal, stromal, and extracellular matrix relationship. This is achieved by an orchestrated involvement of both innate and adaptive immunity. In contrast, normal resolution of acute lung injury may not be achieved. This may actually lead to the pathogenesis of pulmonary fibrosis with features of dysregulated repair with exaggerated neovascularization, fibroproliferation, and abnormal deposition of extracellular matrix, leading to progressive fibrosis and loss of lung function. For example, the host response to a bacterial pneumonia is characterized by an acute inflammatory reaction. The histopathology of bacterial pneumonia is composed of proteinaceous exudate and massive neutrophil extravasation leading to consolidation of the lung. Once the inciting agent is cleared, the inflammatory reaction resolves and normal repair and tissue remodeling occurs. This reestablishes normal lung function without the sequela of chronic pulmonary fibrosis. In contrast, the acute inflammatory response associated with ARDS may culminate in severe lung injury, impacting on resolution of inflammation. This injury may ultimately lead to pulmonary fibrosis, impaired gas transfer, and impact on patient survival. The basic mechanisms and mediators that induce acute pulmonary inflammation remain to be fully elucidated. However, it is known that the participation of a variety of factors, produced by both immune and nonimmune cells, is involved in the coordination of these activities, including reactive oxygen metabolites, carbohydrates, lipids, and protein mediators, such as cytokines.


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