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β2 肾上腺素能调节肥胖和瘦小鼠巨噬细胞的吞噬和杀微生物能力:运动的影响。

β2 Adrenergic Regulation of the Phagocytic and Microbicide Capacity of Macrophages from Obese and Lean Mice: Effects of Exercise.

机构信息

Grupo de Investigación en Inmunofisiología, Departamento de Enfermería, Centro Universitario de Plasencia, Universidad de Extremadura, 10600 Plasencia, Spain.

Instituto Universitario de Investigación Biosanitaria de Extremadura (INUBE), 06071 Badajoz, Spain.

出版信息

Nutrients. 2019 Nov 9;11(11):2721. doi: 10.3390/nu11112721.

DOI:10.3390/nu11112721
PMID:31717554
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6893822/
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.

摘要

巨噬细胞在肥胖相关炎症中起着至关重要的作用。运动是对抗肥胖的主要非药物策略,不仅可以改善代谢障碍,还因为它具有抗炎作用,特别是通过β2 肾上腺素能受体(β2-AR)介导的抗炎作用。然而,这些抗炎作用可能会使先天免疫对病原体攻击的反应受到免疫抑制。因此,本研究的目的是评估肥胖以及肥胖状态下的运动对巨噬细胞先天功能的β2 肾上腺素能调节的影响。使用高脂肪饮食诱导肥胖的 C57BL/6J 小鼠来评估急性运动和规律运动对腹腔巨噬细胞吞噬和杀菌能力的影响。选择性β2-AR 激动剂特布他林(1μM)降低了来自对照瘦型和肥胖型安静动物的巨噬细胞的吞噬和杀菌活性。虽然急性运动没有改变特布他林的抑制能力,但规律运动消除了这种抑制作用。这些影响不能仅通过β2-AR 表面表达的变化来解释。总之,(1)肥胖不会改变β2-AR 介导的巨噬细胞先天反应的降低,(2)规律运动可以逆转特布他林对巨噬细胞吞噬活性的抑制作用,尽管肥胖似乎阻碍了这种免疫生理适应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f96/6893822/6813ef32d307/nutrients-11-02721-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f96/6893822/893c87035c9d/nutrients-11-02721-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f96/6893822/fbaa6ad1b03e/nutrients-11-02721-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f96/6893822/d9b36669de49/nutrients-11-02721-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f96/6893822/6813ef32d307/nutrients-11-02721-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f96/6893822/893c87035c9d/nutrients-11-02721-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f96/6893822/38f6c738b75d/nutrients-11-02721-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f96/6893822/fbaa6ad1b03e/nutrients-11-02721-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f96/6893822/d9b36669de49/nutrients-11-02721-g004.jpg
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