HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Müller, M. Articles by Stridh, H. Search for Related Content PubMed PubMed Citation Articles by Müller, M. Articles by Stridh, H.

Altered apoptosis in bronchoalveolar lavage lymphocytes after allergen exposure of atopic asthmatic subjects

Depts of ¹ Medicine, Division of Respiratory Medicine, and ² Physiology and Pharmacology, Karolinska Institutet and Karolinska University Hospital, and ³ Dept of Oncology and Pathology, Cancer Center Karolinska, Karolinska Institutet, Stockholm, Sweden.

CORRESPONDENCE: M. Müller, Dept of Medicine, Division of Respiratory Medicine, Lung Research Laboratory, L4-01, Karolinska University Hospital, 171 76 Stockholm, Sweden. Fax: 46 851775451. E-mail: malin.muller{at}ki.se

Keywords: Apoptosis, asthma, bronchoalveolar lavage, caspases, lymphocytes, tributyltin

Received: October 10, 2005
Accepted May 20, 2006

The increased number of lymphocytes in airways during an asthmatic response is believed to be the result of increased recruitment of these cells. However, it is possible that a decreased apoptotic rate could also contribute to the increased number. The aim of the present study was to investigate whether allergen airway provocation influences the apoptotic phenotype of lung and peripheral blood lymphocytes (PBL) in subjects with atopic asthma.

Bronchoalveolar lavage (BAL) lymphocytes and PBL from 12 asthmatic subjects previously challenged with allergen (n = 7) or saline (n = 5) were exposed to the apoptotic stimulus tributyltin (TBT) in vitro and assayed for apoptosis.

Airway allergen provocation resulted in decreased sensitivity of BAL lymphocytes to TBT-induced apoptosis, with 42.2% (range 33.9–62.5%) apoptotic cells before challenge versus 23.5% (range 15.3–42.4%) after challenge, while PBL were unaffected. The increased apoptosis resistance correlated with higher numbers of Bcl-2-expressing lymphocytes. Interestingly, baseline caspase-3-like activity was significantly elevated in viable BAL lymphocytes compared with viable PBL, and was unaltered by allergen exposure.

In conclusion, allergen inhalation renders bronchoalveolar lavage lymphocytes more resistant to apoptosis while peripheral blood lymphocytes were not influenced at all, indicating that the apoptotic phenotype of airway lymphocytes may play a role in asthmatic inflammation.