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Originally published online as doi:10.1189/jlb.0703358 on January 23, 2004

Published online before print January 23, 2004
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(Journal of Leukocyte Biology. 2004;75:828-835.)
© 2004 by Society for Leukocyte Biology

Delay of neutrophil apoptosis in acute coronary syndromes

C. D. Garlichs*,1,2, S. Eskafi*,1, I. Cicha*, A. Schmeisser{dagger}, B. Walzog{ddagger}, D. Raaz*, C. Stumpf*, A. Yilmaz*, J. Bremer*, J. Ludwig* and W. G. Daniel*

* Medical Clinic II, Friedrich-Alexander-University of Erlangen-Nürnberg, Germany;
{dagger} Heart Center, Dresden, Germany; and
{ddagger} Department of Physiology, Ludwig-Maximilians-University, Munich, Germany

2Correspondence: Medical Clinic II, Friedrich-Alexander-University of Erlangen-Nürnberg, c/o David-Morgenstern-Weg 14, 91056 Erlangen, Germany. E-mail: Christoph.Garlichs{at}rzmail.uni-erlangen.de

Apoptosis of polymorphonuclear neutrophils (PMN) is currently discussed as a key event in the control of inflammation. This study determined PMN apoptosis and its underlying mechanisms in controls (C), patients with stable (SAP) or unstable angina (UAP), and with acute myocardial infarction (AMI). Blood was drawn from 15 subjects of each C, SAP, UAP, and AMI. Apoptosis was measured by flow cytometry in isolated PMN (propidium iodide staining) and PMN from whole blood (CD16, Fc{gamma}RIII). Serum cytokines were determined by enzyme-linked immunosorbent assay. Apoptosis of isolated PMN was delayed significantly in acute coronary syndromes (ACS) as compared with SAP or C (C, 51.2±12.6%; SAP, 44.9±13.6%; UAP, 28.4±10.1%; AMI, 20.3±8.5%; AMI or UAP vs. SAP or C, P<0.001). These results were confirmed by measurement of PMN apoptosis in cultured whole blood from patients and controls. Moreover, serum of patients with ACS markedly reduced apoptosis of PMN from healthy donors. Analysis of patients’ sera revealed significantly elevated concentrations of tumor necrosis factor {alpha}, interferon-{gamma} (IFN-{gamma}), granulocyte macrophage-colony stimulating factor (GM-CSF), and interleukin (IL)-1ß in ACS (vs. C and SAP). IFN-{gamma}, GM-CSF, and IL-1ß significantly delayed PMN apoptosis in vitro. Furthermore, coincubation of PMN with adenosine 5'-diphosphate-activated platelets significantly inhibited PMN apoptosis as compared with coculture with unstimulated platelets. This study demonstrates a pronounced delay of PMN apoptosis in UAP and AMI, which may result from increased serum levels of IFN-{gamma}, GM-CSF, and IL-1ß and from enhanced platelet activation. Therapeutical modulation of these determinants of PMN lifespan may provide a new concept for the control of inflammation in ACS.

Key Words: inflammation • unstable angina • acute myocardial infarction • leukocytes




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