Regulation of experimental lung inflammation.
Acute lung inflammation is an important component of a number of pulmonary diseases, including acute respiratory distress syndrome (ARDS). Much has been learned about the manner in which various insults to lung, such as infection or trauma, bring about recruitment of neutrophils into alveoli and small airways, resulting in parenchymal damage and organ dysfunction. In this brief review, we discuss the endogenous mechanisms in which the lung regulates the acute inflammatory response in rats to intrapulmonary deposition of IgG immune complexes. Emphasis is given to the participation of the transcription factor, NF-kappaB, in the development of lung injury and the endogenous mediators which attempt to control the extent of lung inflammation by modulating the activation of NF-kappaB.
Lentsch
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AB
Department of Surgery, University of Louisville School of Medicine, Louisville, KY 40202, USA.
Ward
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PA
D000818:Animals; D000936:Antigen-Antibody Complex / Q000008:administration & dosage; D004195:Disease Models, Animal; D006801:Humans; D007074:Immunoglobulin G / Q000008:administration & dosage; D007249:Inflammation / Q000209:etiology* / Q000276:immunology* / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism; D008168:Lung / Q000276:immunology* / Q000378:metabolism; D055370:Lung Injury; D016328:NF-kappa B / Q000378:metabolism; D011480:Protease Inhibitors / Q000378:metabolism; D051381:Rats
D000936:Antigen-Antibody Complex; D007074:Immunoglobulin G; D018836:Inflammation Mediators; D016328:NF-kappa B; D011480:Protease Inhibitors