Regulation of Acute Lung Inflammatory Injury by Endogenous IL-13

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 t...

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Bibliographic Details
Published in:The Journal of immunology (1950) 1999-01, Vol.162 (2), p.1071-1076
Main Authors: Lentsch, Alex B, Czermak, Boris J, Jordan, Jacqueline A, Ward, Peter A
Format: Article
Language:English
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
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Summary: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.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.162.2.1071