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Regulation of Acute Lung Inflammatory Injury by Endogenous IL-13¹

Alex B. Lentsch^*,, Boris J. Czermak, Jacqueline A. Jordan and Peter A. Ward^2,

^* Department of Surgery, University of Louisville School of Medicine, Louisville, KY 40223; Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109; and Department of Trauma Surgery, University of Freiburg, Freiburg, Germany

Using IgG immune complex deposition to trigger acute lung inflammation in rats, we have previously shown that exogenously administered IL-13 suppresses the acute inflammatory response. In the same model, expression of both mRNA and protein for IL-13 has now been detected. Treatment of rats with Ab to IL-13 accentuated the inflammatory response, with significant increases in lung vascular permeability and in the number of neutrophils in bronchoalveolar lavage fluids. In the presence of anti-IL-13, activation of the transcription factor, NF-B, was significantly increased in lung. In addition, anti-IL-13 caused significant increases in bronchoalveolar lavage levels of TNF-, macrophage inflammatory protein-2, and cytokine-inducible neutrophil chemoattractant but no changes in lung vascular ICAM-1. These data suggest that during lung inflammation endogenous IL-13 regulates NF-B activation and related cytokine/chemokine generation, all of which determines the intensity of the lung inflammatory response.

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