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This Article Full Text Full Text (PDF) All Versions of this Article: 107/4/1213    most recent 00316.2009v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted 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 Google Scholar Articles by Wang, J.-S. Articles by Chiu, Y.-T. PubMed PubMed Citation Articles by Wang, J.-S. Articles by Chiu, Y.-T.

Systemic hypoxia enhances exercise-mediated bactericidal and subsequent apoptotic responses in human neutrophils

¹Graduate Institute of Rehabilitation Science and Center for Healthy Aging Research, Chang Gung University, Tao-Yuan; and ; ²Department of Physical Therapy, Dachien General Hospital, Miaoli, Taiwan

Submitted 23 March 2009 ; accepted in final form 24 July 2009

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.

phagocytosis; apoptosis