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Increased production of IL-5 and dominant Th2-type response in airways of Churg-Strauss syndrome patients.

Authors: Jakiela, B  Szczeklik, W  Plutecka, H  Sokolowska, B  Mastalerz, L  Sanak, M  Bazan-Socha, S  Szczeklik, A  Musial, J 
Citation: Jakiela B, etal., Rheumatology (Oxford). 2012 Jul 5.
Pubmed: (View Article at PubMed) PMID:22772323
DOI: Full-text: DOI:10.1093/rheumatology/kes171

Objective. Churg-Strauss syndrome (CSS) is a rare systemic vasculitis associated with eosinophilia and asthma. We assessed the local immune response in airways of CSS patients with different activity of the disease.Methods. Concentration of IL-5, CCL17, CCL22 and CCL26 (ELISA) together with cell expression of T-helper-related genes (real-time PCR array) were measured in bronchoalveolar lavage fluid (BALF) sampled from 11 patients with active CSS, 11 patients with CSS in remission and 9 control subjects with bronchial asthma.Results. In active CSS, both BALF and blood eosinophil counts were increased (P < 0.01). BALF cells in active disease were characterized by an increased expression of Th2 and regulatory-type transcripts: STAT6, STAT3, GATA3, IL4, IL5 and IL10 as compared with asthmatics, and STAT5A, CCR4, FOXP3, IL4, IL5 and IL10 when compared with inactive CSS. There was significant increase in BALF concentration of IL-5 and CCL26 in exacerbation of CSS. CCR4-active chemokines were detected more frequently in active disease. We found a strong positive correlation between clinical parameters of disease activity (BVAS, eosinophilia) and expression of IL4, IL5, IL10 and STAT5A.Conclusion. These results indicate that as compared with asthma, active-CSS patients have much stronger local Th2 response in the airways. Airway cells may contribute to lung eosinophilia in CSS by producing IL-5 and eosinophil active chemokines.

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RGD Object Information
RGD ID: 6892720
Created: 2012-08-14
Species: All species
Last Modified: 2012-08-14
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.