Role of Hsp72 and norepinephrine in the moderate exercise-induced stimulation of neutrophils’ microbicide capacity

Abstract

The influence of a single session of moderate exercise (45 min at 55% of VO(2 )max) performed by young sedentary men (23-25 years old) on the microbicidal capacity of neutrophils was compared by using both direct (killing of phagocytosed Candida albicans) and indirect (superoxide anion production measured by NBT reduction) techniques. In addition, the role of norepinephrine and heat shock protein (Hsp) 72 in the modulation of microbicide capacity of neutrophils was evaluated during the protocol of exercise and recovery period (24 h). No significant changes were found in the superoxide production after exercise. However, immediately after exercise there was an increase in the destruction of C. albicans, which remained higher than basal values 1 day later. This behaviour was similar to the changes found in the serum extracellular Hsp72 concentrations (an increase after exercise that remained higher than basal values 24 h later). In vitro, the raised physiological concentration of Hsp72 after exercise also increased the microbicide capacity of neutrophils with respect to controls and the values induced by the basal concentration of the protein. This indicates that Hsp72 is participating as a "stress mediator" of the stimulated microbicide activity during moderate exercise. However, norepinephrine is not mediating the increased killing of C. albicans during exercise.

Extracellular Hsp72 concentration relates to a minimum endogenous criteria during acute exercise-heat exposure

“…Whitham et al (2006) demonstrated increased eHsp72 was associated with higher plasma levels of catecholamines and heart rate, whilst it has also been observed that following passive heating, neither epinephrine nor norepinephrine was solely responsible for eHsp72 release (Whitham et al 2007). Johnson and Fleshner (2006) identified α-adrenergic stimulation, notably through norepinephrine elevation (Nielsen et al 1997;Ortega et al 2006;Whitham et al 2006;Giraldo et al 2010;Iguchi et al 2012) as responsible for Hsp72 release into the circulation, this alongside the work of Whitham et al (2006Whitham et al ( , 2007 suggest a requirement for individuals to be presented with sustained physiological challenge during exercise-heat stress (Johnson and Fleshner 2006). Exercise intensity, or α-adrenergic stimulation via norepinephrine is likely required to be above an intensity threshold to elicit significant eHsp72 response with the greater exercise intensity data from Périard et al (2012) leading to data contrasting that of Marshall et al (2006).…”

Inflammatory/Stress Feedback Dysregulation in Women with Fibromyalgia

“…FM patients are more prone to C. albicans infections than HW [39], which seems consistent with the increased phagocytic and microbicidal capacities against C. albicans found in the neutrophils from our FM patients. This greater phagocytic and fungicidal capacity (together with a greater chemotactic capacity) of neutrophils could be mediated by the raised circulating concentration of NA and eHsp72 in the FM patients, since it has been reported that increased systemic levels of NA and eHsp72 mediate the stimulation of chemotaxis, phagocytosis and the fungicidal activities of neutrophils [22,40,41,42]. However, the FM group’s decreased latex bead phagocytic capacity (a less specific form of phagocytosis because it is not mediated by pre-opsonization through antibodies) is suggestive of an immunosuppression mediated by the less specific innate immune response carried out by neutrophils.…”

Neuroimmunomodulation during Exercise: Role of Catecholamines as ‘Stress Mediator’ and/or ‘Danger Signal’ for the Innate Immune Response

“…In recent studies on sedentary young men performed in our laboratory based on (1) the direct effect of exercise, (2) evaluation of plasma concentrations of stress hormones and (3) in vitro incubation of neutrophils with the physiological concentrations of these hormones in a basal situation versus the raised levels after exercise, it was concluded that the moderate exercise-induced stimulation of neutrophil phagocytosis is mediated by NA, with the participation of both ␣ -and ␤ -adrenergic receptors [29] . However, although physiological concentrations of NA also stimulated the neutrophil microbicide capacity through both ␣ -and ␤ -receptors, it did not mediate the increased killing of Candida albicans during exercise, this effect being mediated by Hsp72 [30] . The same results for phagocytosis and microbicide capacity after moderate exercise (45 min at 55% VO 2 max on an ergonometric bicycle) were also found in sedentary young women (data not shown).…”