Abstract
Macrophages are crucial in the inflammation associated with obesity. Exercise is the main non-pharmacological strategy against obesity, not only for improving metabolic impairment, but also because of its anti-inflammatory effects, particularly those mediated by β2 adrenergic receptors (β2-AR). Nevertheless, these anti-inflammatory effects could immunocompromise the innate response against pathogen challenge. Thus, the objective of this work was to evaluate the effect of obesity, and of exercise in this condition, on the β2 adrenergic regulation of the innate function of macrophages. High fat diet-induced obese C57BL/6J mice were used to evaluate the effects of acute and regular exercise on the phagocytic and microbicide capacities of peritoneal macrophages. Selective β2-AR agonist terbutaline (1 µM) decreased the phagocytic and microbicide activities of macrophages from control lean and obese sedentary animals. While acute exercise did not modify the inhibitory capacity of terbutaline, regular exercise abolished this inhibitory effect. These effects cannot be explained only by changes in the surface expression of β2-AR. In conclusion, (1) obesity does not alter the β2-AR-mediated decrease of the innate response of macrophages and (2) regular exercise can revert the inhibitory effect of terbutaline on the phagocytic activity of macrophages, although obesity seems to hinder this immunophysiological adaptation.
Highlights
Inflammation is part of the innate immune response mechanisms against pathogens.An appropriate and satisfactory inflammatory response results in the elimination of the infectious agents followed by a resolution and repair phase, which is mediated primarily by resident and recruited macrophages [1]
Phagocytosis and the microbicide activity of macrophages is the “first hurdle” confronting infectious diseases in the body, but it is a key component in regulating innate and adaptive immune function [2]. It is well-known that both obesity [3] and exercise [4,5] affect the innate/inflammatory immune response mediated by macrophages, and that neuroimmunomodulation participates in these responses mainly through catecholamines [6,7]
The β2 adrenergic receptors (β2-adrenergic receptors (AR)) agonist terbutaline decreases the phagocytic and microbicide capacities of peritoneal macrophages in sedentary animals, and obesity does not alter this β2-AR neuroimmunomodulation of macrophages
Summary
Inflammation is part of the innate immune response mechanisms against pathogens.An appropriate and satisfactory inflammatory response results in the elimination of the infectious agents followed by a resolution and repair phase, which is mediated primarily by resident and recruited macrophages [1]. Phagocytosis and the microbicide activity of macrophages is the “first hurdle” confronting infectious diseases in the body, but it is a key component in regulating innate and adaptive immune function [2] It is well-known that both obesity [3] and exercise [4,5] affect the innate/inflammatory immune response mediated by macrophages, and that neuroimmunomodulation participates in these responses mainly through catecholamines [6,7]. It had been shown that the obese Zucker rat (a common animal model of metabolic syndrome) presents a dysregulation in the feedback mechanism between inflammatory cytokines and noradrenaline (NA), and that the regulation of the macrophage-derived cytokines by NA and phagocytic activity is defective in these animals This could contribute to the low-grade inflammation and greater susceptibility to infections associated with obesity [7,14,15]. Changes in the recruitment and activation of macrophages in the adipose tissue contribute fundamentally to the regulation of metabolic homeostasis, and a pathogenic or protective role of macrophages depending on their profile in experimental models of obesity has been suggested [16,17]
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