Cytokines and adhesion molecules in the lung inflammatory response

Abstract

Intrapulmonary deposition of IgG immune complexes in rat lung triggers a series of inflammatory responses that result in acute lung injury involving vascular endothelial cells, alveolar epithelial cells and connective tissue matrix. Understanding of these pathophysiological events may yield information for human inflammatory diseases such as rheumatoid arthritis, systemic lupus erythematosus, membranous nephritis and systemic vasculitis, all of which are characterized by deposition of IgG immune complexes together with complement activation products. The IgG immune complex model of acute lung injury in rats is triggered by the airway instillation of rabbit polyclonal antibody (IgG) against bovine serum albumin (BSA) followed by the intravenous infusion of BSA. The inflammatory response (neutrophil accumulation) and evidence of injury (leakage of [125I]albumin and haemorrhage) reaches a maximum at 4h and then, for reasons not fully understood, undergoes remission. The availability of complement and the accumulation of neutrophils are central to the development of injury. Adhesion molecules, both on endothelial cells and on leukocytes themselves, play an important role in the inflammatory outcome.