Document Detail


Exercise delays neutrophil apoptosis by a G-CSF-dependent mechanism.
MedLine Citation:
PMID:  22858628     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The aim of the study was to determine whether exercise affects neutrophil apoptosis and to characterize the underlying mechanisms. Using annexin V labeling, neutrophil apoptosis was measured using flow cytometry after various bouts of exercise (marathon run, concentric/eccentric treadmill exercise, moderate/intensive resistance training) and in vitro conditions. Similarly, apoptosis-related markers as death receptors/ligands and mitochondrial membrane potential were detected. Furthermore, concentrations of intracellular free calcium and glutathione were measured using spectrofluorometry. After both marathon run and intensive laboratory exercise tests, neutrophil apoptosis was delayed. Furthermore, neutrophils mitochondrial membrane potential and death receptor/ligand expression were not affected by exercise. Apoptosis delay was accompanied under some exercise conditions by enhanced intracellular calcium transients and decreased glutathione levels. A delay of spontaneous apoptosis in vitro could be induced by incubation of neutrophils in postexercise serum. Heating of postexercise serum abolished the apoptosis delaying effect. In vitro stimulation of resting neutrophils with granulocyte-colony-stimulating factor (G-CSF) and C-reactive protein resulted in apoptosis delay too. Addition of anti-G-CSF antibody to postexercise serum was also effective in reversing its apoptosis-delaying effect. Exercise-induced mobilization of neutrophils is associated with a delay of apoptosis. This fundamental process seems to maintain exercise-induced neutrophilia and to contribute to the alerting and activation of the nonadaptive immune system known from other inflammatory conditions. An important extracellular trigger of apoptosis delay during exercise conditions seems to be G-CSF; intracellular processes may include calcium and redox signaling.
Authors:
Frank C Mooren; Klaus Völker; Rainer Klocke; Sigrid Nikol; Johannes Waltenberger; Karsten Krüger
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Publication Detail:
Type:  Journal Article     Date:  2012-08-02
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  113     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-10-02     Completed Date:  2013-05-23     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1082-90     Citation Subset:  IM    
Affiliation:
Department of Sports Medicine, Institute of Sports Sciences, Justus-Liebig-University Giessen, Kugelberg 62, Giessen, Germany. Frank-Christoph.Mooren@sport.uni-giessen.de
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MeSH Terms
Descriptor/Qualifier:
Annexin A5 / metabolism
Apoptosis / physiology*
C-Reactive Protein / metabolism
Calcium / metabolism
Exercise / physiology*
Glutathione / metabolism
Granulocyte Colony-Stimulating Factor / blood,  metabolism*
Humans
Immune System / metabolism,  physiopathology
Inflammation / metabolism,  physiopathology
Ligands
Male
Membrane Potential, Mitochondrial / physiology
Neutrophils / physiology*
Receptors, Death Domain / metabolism
Running
Signal Transduction / physiology
Chemical
Reg. No./Substance:
0/Annexin A5; 0/Ligands; 0/Receptors, Death Domain; 143011-72-7/Granulocyte Colony-Stimulating Factor; 70-18-8/Glutathione; 7440-70-2/Calcium; 9007-41-4/C-Reactive Protein

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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