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Tumor necrosis factor-alpha and interleukin-1 alpha expression in a murine model of allergic bronchopulmonary aspergillosis.

Authors: Chu, HW  Wang, JM  Boutet, M  Laviolette, M 
Citation: Chu HW, etal., Lab Anim Sci. 1996 Feb;46(1):42-7.
Pubmed: (View Article at PubMed) PMID:8699818

Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 alpha (IL-1 alpha) are two important proinflammatory cytokines that may be involved in allergic inflammatory processes. We recently developed a murine model of allergic bronchopulmonary aspergillosis characterized by eosinophilic and lymphocyte lung infiltration and increased serum and bronchoalveolar lavage immunoglobulin E concentration. In this study we examined the expression of TNF-alpha and IL-1 alpha in the lung tissue sections of C57BL/6 mice that were intranasally challenged with Aspergillus fumigatus antigen or saline on the first 3 days of each week and sacrificed on days 4, 7, 14, and 21. Compared with the control mice, A. fumigatus treated mice had a remarkable increase of TNF-alpha and IL-1 alpha expression in the lung on days 4, 14, and 21, with a slight increase on day 7. The major types of cells expressing TNF-alpha and IL-1 alpha included alveolar macrophages, endothelial cells, and bronchiolar and alveolar epithelial cells. Consistent with increased expression of TNF-alpha and IL-1 alpha, intercellular adhesion molecule-1 expression also was upregulated in the lung of A. fumigatus treated mice; its time course and cell types were similar to those of TNF-alpha and IL-1 alpha expression. These results suggest that TNF-alpha and IL-1 alpha may be involved in the A. fumigatus induced inflammatory process and that upregulated intercellular adhesion molecule-1 expression may represent one of the roles played by TNF-alpha and IL-1 alpha in this murine model.

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CRRD Object Information
CRRD ID: 7794730
Created: 2014-01-08
Species: All species
Last Modified: 2014-01-08
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.