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Elevated expression of TARC (CCL17) and MDC (CCL22) in models of cigarette smoke-induced pulmonary inflammation.

Authors: Ritter, M  Goggel, R  Chaudhary, N  Wiedenmann, A  Jung, B  Weith, A  Seither, P 
Citation: Ritter M, etal., Biochem Biophys Res Commun. 2005 Aug 19;334(1):254-62.
Pubmed: (View Article at PubMed) PMID:15993846
DOI: Full-text: DOI:10.1016/j.bbrc.2005.06.084

TARC (CCL17) and MDC (CCL22) are well-known chemoattractants for Th2 cells. Here, we evaluated the role of both chemokines for cigarette smoke-induced airway inflammation. The expression profiles of MDC, TARC, and their receptor CCR4 were analyzed in models of acute and chronic cigarette smoke-induced airway inflammation that is characterized by a Th1 immune response. The results were compared to the expression of both chemokines in models of idiopathic pulmonary fibrosis and acute asthma, which are associated with a Th2 immune response. The expression of MDC and TARC was found to be elevated in all lung inflammation models. In contrast to the findings in the asthma and lung fibrosis models, the increased expression of MDC and TARC in the cigarette-smoke model was not associated with an increased infiltration of Th2 cells into smoke-treated lungs. Our data indicate that instead of Th2 cells, airway epithelial cells expressing CCR4 might be the principal targets for MDC and TARC released from alveolar macrophages during cigarette smoke-induced airway inflammation.

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CRRD Object Information
CRRD ID: 2306304
Created: 2009-04-08
Species: All species
Last Modified: 2009-04-08
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.