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Regulation of acute lung inflammatory injury by endogenous IL-13.

Authors: Lentsch, AB  Czermak, BJ  Jordan, JA  Ward, PA 
Citation: Lentsch AB, etal., J Immunol. 1999 Jan 15;162(2):1071-6.
Pubmed: (View Article at PubMed) PMID:9916735

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.


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CRRD Object Information
CRRD ID: 4145650
Created: 2010-11-11
Species: All species
Last Modified: 2010-11-11
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.