Norepinephrine as mediator in the stimulation of phagocytosis induced by moderate exercise

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Background: It is still not really known what is the optimal level of exercise that improves, but does not impair or overstimulate the innate immune function. This is especially the case in women, who have higher basal levels of ‘inflammatory markers’ than men. The aim of this work was to evaluate differences in the magnitude of the stimulation of the innate/inflammatory response following a single bout of moderate or intense exercise in sedentary women, all of them in the follicular phase of their menstrual cycle. Changes in stress and sexual hormones were also evaluated. Methods: Changes induced by exercise (45 min at 55% VO₂ max vs. 1 h at 70% VO₂ max on a cycle ergometer) in the phagocytic process (chemotaxis, phagocytosis, and microbicide capacity against Candida albicans) and in serum concentrations of IL-1β, IL-2, IFN-γ, IL-12, IL-6, and IL-4 (ELISA) were evaluated. Parallel determinations were also made of serum or plasma concentrations of catecholamines (HPLC) and cortisol, oestradiol, and progesterone (electrochemiluminescence immunoassay). Results: Both exercise intensities increased chemotaxis, phagocytosis, and microbicide capacity of the neutrophils. However, the increase in chemotaxis was greater after moderate exercise. All the cytokines assayed were affected by exercise intensity. IFN-γ increased significantly only immediately after the intense exercise; IL-1β increased following both exercise intensities, although at 24 h it only remained elevated after the intense exercise; IL-12 only increased 24 h after the intense exercise, and IL-2 only showed a significant decrease following the moderate exercise. IL-6 increased immediately after both exercise intensities, but more so after moderate exercise. While IL-4 (an anti-inflammatory cytokine) increased following the moderate exercise, it decreased after the intense exercise. Both moderate and intense exercise increased norepinephrine and decreased cortisol, both of which returned to basal levels after 24 h. Only the intense exercise affected the epinephrine, oestradiol, and progesterone concentrations, with increases in epinephrine and oestradiol immediately after exercise, and a decrease in progesterone after 24 h. Conclusions: Both moderate and intense exercise stimulate the phagocytic process of neutrophils in sedentary women, but the profile of pro-/anti-inflammatory cytokine release seems to be better following the moderate exercise. The possible participation of stress (catecholamines and cortisol) and sex (oestradiol and progesterone) hormones in these intensity-dependent immune changes is discussed.

Section: Discussionmentioning

confidence: 99%

Exercise Intensity-Dependent Changes in the Inflammatory Response in Sedentary Women: Role of Neuroendocrine Parameters in the Neutrophil Phagocytic Process and the Pro-/Anti-Inflammatory Cytokine Balance

Giraldo

Garcı́a

Hinchado

et al. 2009

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“…Catecholamines could have opposite effects on phagocytosis depending on their concentration, as demonstrated by Roy and Rai [30] . High-dose catecholamine treatment decreases polymorphonuclear leukocyte phagocytic capacity [31] ; however, there are some reports of stimulation of phagocytosis by norepinephrine at similar concentrations [32,33] . These studies suggest that the effect depends on the concentrations and possibly on the number or type of adrenoreceptors [30,[32][33][34][35] .…”

Section: Discussionmentioning

confidence: 99%

“…High-dose catecholamine treatment decreases polymorphonuclear leukocyte phagocytic capacity [31] ; however, there are some reports of stimulation of phagocytosis by norepinephrine at similar concentrations [32,33] . These studies suggest that the effect depends on the concentrations and possibly on the number or type of adrenoreceptors [30,[32][33][34][35] . Moreover, macrophages under the influence of high levels of catecholamines, as after LPS injection, can exhibit different types and numbers of adrenoreceptors since their expression can change during immunological activation [36][37][38][39] .…”

Section: Discussionmentioning

confidence: 99%

Effects of Cold Stress, Corticosterone and Catecholamines on Phagocytosis in Mice: Differences between Resting and Activated Macrophages

Baccan

Sesti-Costa

Chedraoui-Silva

et al. 2010

Objective: We subjected mice to acute cold stress and studied the effect on phagocytosis by peritoneal macrophages mediated by 3 types of phagocytic receptors: Fcγ, complement receptors 3 (CR3) and mannose and β-glucan receptors. Methods: Mice were subjected to a cold stress condition (4°C for 4 h), and then peritoneal macrophages were harvested and phagocytosis assays performed in vitro. Results: We found a striking difference between resting and lipopolysaccharide (LPS)-activated macrophages (by intraperitoneal injection of LPS 4 days before the stress experiment): for resting macrophages cold stress caused a decrease in phagocytosis mediated by Fcγ or mannose receptors, while for activated macrophages we observed an increase in phagocytosis by the 3 types of receptors. These effects were associated with an increase in plasma concentrations of corticosterone and catecholamines following the cold stress. In order to verify whether these hormone changes could account for the observed effects on phagocytosis, we performed in vitro assays by incubating macrophages harvested from nonstressed animals with these hormones for 4 h at 37°C and measuring their phagocytic capacity. The following experiments were done: (a) with resting (nonactivated) macrophages; (b) with macrophages previously activated in vitro by incubation with LPS; (c) with macrophages previously activated in vivo by intraperitoneal injection of mice with LPS, 4 days before harvesting the cells. We found that for resting macrophages, corticosterone decreased phagocytosis mediated by Fcγ and mannose and β-glucan receptors, but catecholamines had no effect. For macrophages activated either in vivo or in vitro, catecholamines caused an increase in phagocytosis (excluding mannose receptors) while corticosterone had no effect. Conclusion: The above findings suggest that stress can regulate phagocytosis in different ways, depending on the kind of phagocytic receptor involved, the level of stress hormones and the physiological state of the macrophages.

“…For example, when adrenaline was used in concentrations equal to those induced by intense exercise, no significant changes in phagocytosis or candidicidal activity of isolated neutrophils were found [28] . 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] .…”

Section: Catecholamines As Neuroendocrine Mediator In the Modulation mentioning

confidence: 99%

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

Ortega

Giraldo

Hinchado

et al. 2007

Exercise-induced neuroimmunomodulation is clearly accepted today. The present article reviews the main literature concerning the immunomodulatory capacity of catecholamines on the innate immune response during physical exercise, and presents our laboratory’s latest results on this topic. It is well known that the effects of exercise on the immune system are mediated by the ‘stress hormones and mediators’. Although catecholamines have usually been regarded as immunosuppressors, they may stimulate innate immune response mechanisms (such as phagocytic function) during exercise-induced stress, even without previous antigenic stimulation. The exercise-induced stimulation of the phagocytic response in particular and the innate responses in general have been considered as a prevention strategy of the athlete’s organism in order to prevent the entry and/or maintenance of antigens in a situation where the adaptive immune response seems to be depressed, and thus it has been suggested that catecholamines participate as a ‘stress mediator’ of these effects. Given this hypothesis, it is also suggested here that catecholamines may be the first ‘danger signal’ to the immune system during exercise-induced stress.