Skip Navigation


Rheumatology Advance Access originally published online on July 29, 2009
Rheumatology 2009 48(10):1202-1207; doi:10.1093/rheumatology/kep209
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplementary Data
Right arrow All Versions of this Article:
48/10/1202    most recent
kep209v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Jakiela, B.
Right arrow Articles by Szczeklik, A.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jakiela, B.
Right arrow Articles by Szczeklik, A.
Related Collections
Right arrow Vasculitis
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Intrinsic pathway of apoptosis in peripheral blood eosinophils of Churg–Strauss syndrome

Bogdan Jakiela1, Wojciech Szczeklik1, Barbara Sokolowska1, Lucyna Mastalerz1, Marek Sanak1, Hanna Plutecka1 and Andrzej Szczeklik1

1Department of Medicine, Jagiellonian University Medical College, Krakow, Poland.

Correspondence to: Andrzej Szczeklik, Department of Medicine, Jagiellonian University Medical College, ul. Skawinska 8, 31-066 Krakow, Poland. E-mail: mmszczek{at}cyf-kr.edu.pl


  Abstract

Objectives. Churg–Strauss syndrome (CSS) is a rare necrotizing vasculitis associated with asthma, blood and tissue eosinophilia and granuloma formation. We wondered whether eosinophil accumulation in CSS results from the defect of intrinsic apoptosis pathway in blood eosinophils, leading to their prolonged survival.

Methods. We analysed immunophenotype (flow cytometry), expression of apoptosis-related genes (real-time PCR) and spontaneous apoptosis in blood eosinophils isolated from nine patients in exacerbation (active CSS), seven patients in remission (inactive CSS) and 14 matched healthy subjects. Serum IL-5 levels were also measured.

Results. In active CSS, blood eosinophils were characterized by small (<2-fold) decrease in expression of a few genes, primarily proapoptotic (e.g. BCL2L13, CASP2, CARD4) or involved in regulation of NF-{kappa}B (IKBKB, REL), but they did not differ in the rate of spontaneous apoptosis, when compared with other groups. Only selected genes were positively (BNIPL, PYCARD, CASP8, CRADD, BCAP31), or negatively (IKBKE) correlated with disease activity. In active CSS, eosinophils expressed activation markers (CD69, CD25), especially in subjects with most severe disease and elevated serum IL-5.

Conclusions. High susceptibility of peripheral blood eosinophils to spontaneous apoptosis in vitro, and minor changes in expression of apoptotic-related genes in transcriptome analysis, do not support the hypothesis on intrinsic defect in apoptosis, as the cause of eosinophil accumulation in CSS.

KEY WORDS: Churg–Strauss syndrome, Eosinophil, Apoptosis, Gene expression

Submitted 8 April 2009; revised version accepted 17 June 2009.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.