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Prepublished online as a Blood First Edition Paper on September 12, 2002; DOI 10.1182/blood-2002-01-0239. This Article Full Text (PDF) All Versions of this Article: 2002-01-0239v1 101/2/739    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Weinmann, P. Articles by Walzog, B. Search for Related Content PubMed PubMed Citation Articles by Weinmann, P. Articles by Walzog, B. Social Bookmarking                   What's this? Submitted January 25, 2002 Accepted August 21, 2002 A role for apoptosis in the control of neutrophil homoeostasis in the circulation: insights from CD18-deficient mice Pamela Weinmann, Karin Scharffetter-Kochanek, S Bradley Forlow, Thorsten Peters, and Barbara Walzog* Department of Physiology, Freie Universitaet, Berlin, Germany Department of Dermatology and Allergology, Universitaet Ulm, Ulm, Germany Department of Biomedical Engineering, University of Virginia School of Medicine, Charlottesville, VA, USA Department of Dermatology, Universitaet zu Koeln, Koeln, Germany Department of Physiology, Ludwig-Maximilians-Universitaet, Muenchen, Germany * Corresponding author; email: walzog{at}lrz.uni-muenchen.de. The control of neutrophil turnover in the circulation is a key event in homoeostasis and inflammation. Using CD18-deficient (CD18-/-) mice which show a 19-fold increase of blood neutrophil counts when compared to wild-type animals (CD18+/+), we found that apoptosis of peripheral neutrophils was significantly reduced from 27.4% in the wild-type to 4.8% in CD18-/- mice within 4 h after isolation as measured by analysis of DNA content. This was confirmed by detecting CD16 expression, nuclear morphology, and internucleosomal DNA degradation. In contrast, no difference in apoptosis was observed in neutrophils derived from the bone marrow. Neutrophilia and delayed neutrophil apoptosis was also present in CD18-/-/IL6-/- double knockout mice. Moreover, plasma of CD18-/- mice was not able to delay apoptosis of CD18+/+ neutrophils and plasma of CD18+/+ mice did not augment apoptosis of CD18-/- neutrophils. However, CD18-/- neutrophils revealed an up-regulation of the anti-apoptotic gene bcl-Xl and a down-regulation of the pro-apoptotic gene bax- compared to CD18+/+ neutrophils suggesting that this delayed apoptosis. Accordingly, down-regulation of Bax- using antisense technique delayed apoptosis and prolonged neutrophil survival. The replacement of the hematopoietic system of CD18+/+ mice by a 1:1 mixture of CD18+/+ and CD18-/- hematopoietic cells abolished the delay of apoptosis in peripheral CD18-/- neutrophils and prevented neutrophilia. Altogether, this suggests that a delay of neutrophil apoptosis in CD18-/- mice causes an alteration of neutrophil homoeostasis which may induce the massive increase of peripheral neutrophil counts. Thus, apoptosis seems to be critically involved in the control of neutrophil turnover in the circulation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? 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