Regulation of Acute Lung Inflammatory Injury by Endogenous IL-13

• Published in: The Journal of immunology (1950) Vol. 162; no. 2; pp. 1071 - 1076
• Main Authors: Lentsch, Alex B, Czermak, Boris J, Jordan, Jacqueline A, Ward, Peter A
• Format: Journal Article
• Language: English
• Published: United States Am Assoc Immnol 15.01.1999
• Subjects: Acute Disease; Adjuvants, Immunologic - administration & dosage; Alveolitis, Extrinsic Allergic - etiology; Alveolitis, Extrinsic Allergic - immunology; Alveolitis, Extrinsic Allergic - pathology; Animals; Antigen-Antibody Complex - toxicity; Bronchoalveolar Lavage Fluid - immunology; Chemokines, CXC - metabolism; Immune Sera - administration & dosage; Immunoglobulin G - toxicity; Intercellular Adhesion Molecule-1 - biosynthesis; Intercellular Adhesion Molecule-1 - blood; Intercellular Adhesion Molecule-1 - metabolism; Interleukin-13 - biosynthesis; Interleukin-13 - immunology; Interleukin-13 - physiology; Intubation, Intratracheal; Lung - blood supply; Lung - metabolism; Male; NF-kappa B - metabolism; Rats; Rats, Long-Evans; Tumor Necrosis Factor-alpha - metabolism
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.162.2.1071

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-kappaB, was significantly increased in lung. In addition, anti-IL-13 caused significant increases in bronchoalveolar lavage levels of TNF-alpha, 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-kappaB activation and related cytokine/chemokine generation, all of which determines the intensity of the lung inflammatory response.