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The transcription factor early growth-response factor 1 modulates tumor necrosis factor-alpha, immunoglobulin E, and airway responsiveness in mice.

Authors: Silverman, ES  De Sanctis, GT  Boyce, J  MacLean, JA  Jiao, A  Green, FH  Grasemann, H  Faunce, D  Fitzmaurice, G  Shi, GP  Stein-Streilein, J  Milbrandt, J  Collins, T  Drazen, JM 
Citation: Silverman ES, etal., Am J Respir Crit Care Med. 2001 Mar;163(3 Pt 1):778-85.
Pubmed: (View Article at PubMed) PMID:11254538
DOI: Full-text: DOI:10.1164/ajrccm.163.3.2003123

Early growth-response factor 1 (Egr-1) is a sequence-specific transcription factor that plays a regulatory role in the expression of many genes important in inflammation, cell growth, apoptosis, and the pathogenesis of disease. In vitro studies suggest that Egr-1 is capable of regulating the expression of tumor necrosis factor-alpha (TNF-alpha) and other genes involved in airway inflammation and reactivity following allergen stimulation. On the basis of these data, we hypothesized that in the absence of Egr-1, the TNF-alpha response and subsequent downstream inflammatory events that usually follow allergen challenge would be diminished. To test our hypothesis Egr-1 knock-out (KO) mice were examined in an ovalbumin (OVA)-induced model of airway inflammation and reactivity, and compared with identically treated wild-type (WT) control mice. In response to OVA sensitization and airway challenge, KO mice had diminished TNF-alpha mRNA and protein in the lungs and mast cells compared with WT mice. Interestingly, the KO mice had elevated IgE levels at baseline and after allergen challenge compared with WT mice. Furthermore, the airways of KO mice were hyporesponsive to methacholine challenge at baseline and after allergen challenge. These data indicate that Egr-1 modulates TNF-alpha, IgE, and airway responsiveness in mice.

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CRRD Object Information
CRRD ID: 5131985
Created: 2011-05-17
Species: All species
Last Modified: 2011-05-17
Status: ACTIVE



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