Journal of Applied Physiology AJP: Regulatory, Integrative and Comparative Physiology
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J Appl Physiol (September 13, 2002). doi:10.1152/japplphysiol.00681.2002
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Articles in PresS, published online ahead of print September 13, 2002
J Appl Physiol, 10.1152/jap.00681.2002
Submitted on July 25, 2002
Accepted on September 9, 2002

The role of extracellular HSP72 in acute stress-induced potentiation of innate immunity in physically active rats

Jay Campisi1 and Monika Fleshner1*

1 Department of Kinesiology and Applied Physiology, University of Colorado at Boulder, Boulder, CO, USA; Center for Neuroscience, University of Colorado at Boulder, Boulder, CO, USA

* To whom correspondence should be addressed. E-mail: fleshner{at}colorado.edu.

Acute stress can both compromise acquired, and potentiate innate, immunity. Recent evidence suggests that impact of stress on measures of immunity can be modulated by the physical activity status of the organism, and that extracellular heat-shock protein72 (eHSP72) contributes to the activation of innate immunity produced by stress. Therefore, this study investigated if physical activity status would impact the immunologically enhancing effects of stressor exposure (inescapable tailshock stress; IS) on innate immunity, and if changes in eHSP72 responses could play a role. Adult, male Fischer 344 rats (5/grp) lived with either mobile (physically active) or immobile (sedentary) running wheels. After 6 wks, rats were exposed to either IS (100, 1.6 mA tailshocks, 5-sec duration, 60-sec ITI) or no stress. Immediately following IS all rats were injected subcutaneously with live Escherichia coli (E. coli; ATCC 15746 ~2.5x109 CFU). Inflammation diameter and grade were measured daily and plasma eHSP72 was measured at various time points. Rats exposed to IS resolved their inflammation faster than nonstressed rats, but the beneficial impact of stress on recovery was greater in physically active rats. All rats had equal increases in the concentration of circulating eHSP72 following IS. In a separate cohort of nonstressed physically active and sedentary rats, spleen cells (5x106/ml) were cultured with media, eHSP72 or lipopolysaccharide. Nitric oxide and pro-inflammatory cytokines were measured. Physically active rats responded to eHSP72 stimulation in vitro with a greater nitric oxide and cytokine response than sedentary rats. Thus, physically active rats both recover faster than sedentary rats following bacterial challenge + IS exposure, and demonstrate potentiated cellular responses to eHSP72 activation that could be important for bacterial recovery.




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