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This Article 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 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 Colotta, F. Articles by Mantovani, A. Search for Related Content PubMed PubMed Citation Articles by Colotta, F. Articles by Mantovani, A. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Modulation of granulocyte survival and programmed cell death by cytokines and bacterial products F Colotta, F Re, N Polentarutti, S Sozzani and A Mantovani Istituto di Ricerche Farmacologiche Mario Negri, Centro Daniela e Catullo Borgomainerio, Milano, Italy. Mature circulating polymorphonuclear cells (PMN) have the shortest half- life among leukocytes and undergo rapid programmed cell death in vitro. In this study, we have examined the possibility that inflammatory signals (cytokines and bacterial products) can regulate PMN survival. PMN in culture were found to rapidly die, with percentages of survival at 24, 48, 72, and 96 hours of 97.3% +/- 1.9%, 36.8% +/- 5.3%, 14.5% +/- 3.1%, and 4.2% +/- 2.9%, respectively (mean +/- SE of 20 different donors). PMN incubated with interleukin-1 beta (IL-1 beta), tumor necrosis factor, granulocyte-macrophage colony-stimulating factor (CSF), granulocyte-CSF, and interferon-gamma (IFN-gamma), but not with prototypic chemoattractants (fMLP, recombinant C5a, and IL-8), showed a marked increase in survival, with values ranging at 72 hours of incubation from 89.5% +/- 5.8% for IL-1 beta to 47.6% +/- 6.4% for IFN- gamma. The calculated half-life was 35 hours for untreated and 115 hours for IL-1-treated PMN. PMN activated with lipopolysaccharide (LPS) or inactivated streptococci also showed a longer survival compared with untreated cells (94.4% +/- 3.2% and 95.5% +/- 2.4%, respectively, at 72 hours). PMN surviving in response to LPS or IL-1 beta retained the capacity to produce superoxide anion when treated with phorbol esters or fMLP. All inducers of PMN survival protect these cells from programmed cell death because they reduced cells with morphologic features of apoptosis and the fragmentation of DNA in multiples of 180 bp. Thus, certain cytokines and bacterial products can prolong PMN survival by interfering with the physiologic process of apoptosis. Prolongation of survival may be important for the regulation of host resistance and inflammation, and may represent a crucial permissive step for certain cytokines and microbial products that activate gene expression and function in PMN. Volume 80, Issue 8, pp. 2012-2020, 10/15/1992 Copyright © 1992 by The American Society of Hematology CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: L. M. Biasucci, G. Liuzzo, S. Giubilato, R. Della Bona, M. Leo, M. Pinnelli, A. Severino, M. Gabriele, S. Brugaletta, M. Piro, et al. Delayed neutrophil apoptosis in patients with unstable angina: relation to C-reactive protein and recurrence of instability Eur. Heart J., September 2, 2009; 30(18): 2220 - 2225. [Abstract] [Full Text] [PDF] Z. Mikhak, A. Farsidjani, and A. D. Luster Endotoxin Augmented Antigen-Induced Th1 Cell Trafficking Amplifies Airway Neutrophilic Inflammation J. Immunol., June 15, 2009; 182(12): 7946 - 7956. [Abstract] [Full Text] [PDF] A. Drewniak, B. J. van Raam, J. Geissler, A. T.J. Tool, O. R.F. Mook, T. K. van den Berg, F. Baas, and T. W. 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