Document Detail

Systemic hypoxia enhances exercise-mediated bactericidal and subsequent apoptotic responses in human neutrophils.
MedLine Citation:
PMID:  19644031     Owner:  NLM     Status:  MEDLINE    
Phagocytosis and oxidative burst are critical host defense mechanisms in which neutrophils clear invading pathogens. Clearing phagocytic neutrophils by triggering apoptosis is an essential process for controlling inflammation. This study elucidates how various exercise bouts with/without hypoxia affected neutrophil bactericidal activity and subsequent apoptosis in humans. Fifteen sedentary males performed six distinct experimental tests in an air-conditioned normobaric hypoxia chamber: two normoxic exercises [strenuous exercise (SE; up to maximal O2 consumption) and moderate exercise (ME; 50% maximal O2 consumption for 30 min) while exposed to 21% O2], two hypoxic exercises (ME for 30 min while exposed to 12% and 15% O2), and two hypoxic exposures (resting for 30 min while exposed to 12% and 15% O2). The results showed that 1) plasma complement-C3a desArg/C4a desArg/C5a concentrations were increased, 2) expressions of L-selectin/lymphocyte functin-associated antigen-1/Mac-1/C5aR on neutrophils were enhanced, 3) phagocytosis of neutrophils to Esherichia coli and release of neutrophil oxidant products by E. coli were elevated, and 4) E. coli-induced phosphotidylserine exposure or caspase-3 activation of neutrophils were promoted immediately and 2 h after both 12% O2 exposure at rest and with ME as well as normoxic SE. Although neither normoxic ME nor breathing 15% O2 at rest influenced these complement- and neutrophil-related immune responses, ME at both 12% and 15% O2 resulted in enhanced complement activation in the blood, expressions of opsonic/complement receptors on neutrophils, or the bactericidal activity and apoptosis of neutrophils. Moreover, the increased neutrophil oxidant production and apoptosis by normoxic SE and hypoxic ME were ameliorated by treating neutrophils with diphenylene iodonium (a NADPH oxidase inhibitor). Therefore, we conclude that ME at 12-15% O2 enhances bactericidal capacity and facilitates the subsequent apoptosis of neutrophils.
Jong-Shyan Wang; Ya-Ting Chiu
Publication Detail:
Type:  Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't     Date:  2009-07-30
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  107     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2009 Oct 
Date Detail:
Created Date:  2009-10-16     Completed Date:  2009-12-24     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:  1213-22     Citation Subset:  IM    
Graduate Institute of Rehabilitation Science, Chang Gung Univ., 259 Wen-Hwa 1st Rd., Kwei-Shan, Tao-Yuan 333, Taiwan.
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MeSH Terms
Anoxia / immunology,  microbiology*,  pathology,  physiopathology
Apoptosis* / drug effects
Biological Markers / blood
Blood Bactericidal Activity* / drug effects
Caspase 3 / metabolism
Complement C3a / metabolism
Complement C4a / metabolism
Complement C5a, des-Arginine / metabolism
Enzyme Activation
Enzyme Inhibitors / pharmacology
Escherichia coli / pathogenicity*
L-Selectin / blood
Lymphocyte Function-Associated Antigen-1 / blood
Macrophage-1 Antigen / blood
NADPH Oxidase / antagonists & inhibitors,  metabolism
Neutrophils / drug effects,  immunology,  microbiology*,  pathology
Onium Compounds / pharmacology
Oxygen Consumption
Phagocytosis* / drug effects
Phosphatidylserines / metabolism
Receptors, Complement / blood
Respiratory Burst* / drug effects
Time Factors
Young Adult
Reg. No./Substance:
0/Biological Markers; 0/C5AR1 protein, human; 0/Complement C5a, des-Arginine; 0/Enzyme Inhibitors; 0/Lymphocyte Function-Associated Antigen-1; 0/Macrophage-1 Antigen; 0/Onium Compounds; 0/Phosphatidylserines; 0/Receptors, Complement; 0/complement C4a, des-Arg; 126880-86-2/L-Selectin; 244-54-2/diphenyleneiodonium; 80295-42-7/Complement C3a; 80295-49-4/Complement C4a; EC Oxidase; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/Caspase 3

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

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