Abstract

Neutrophils play important roles in host defense against infectious agents but, paradoxically, they are also involved in the pathology of various inflammatory conditions. Their microbicidal armory consists of oxidative and nonoxidative processes that are activated simultaneously upon phagocytosis. While destruction of infectious agents occurs intracellularly, release of cytotoxic molecules into the extracellular milieu can damage body tissues. Neutrophils are not a homogeneous cell population. Subpopulations exist in various stages from dormant to primed to fully activated. The activities of neutrophils are modulated by cytokines, hormones and bioactive lipids. As neutrophils represent 60% of the circulating leukocyte pool, they are readily accessible to experimental investigation. The sequence of events that occurs in the neutrophil response to microbial invasion includes adherence, chemotaxis, phagocytosis, the oxidative burst, degranulation and microbial killing. In general, high-intensity exercise suppresses most neutrophil functions both acutely and chronically while the effects of moderate exercise have been conflicting. This review will summarize where the field is now and present some suggestions for future research. Emphasis will be placed on resolving conflicting results that may be due to biological and technical variability, and determination of the regulatory events that may mediate exercise-induced changes in neutrophil function.

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