Macrophage polarization: implications on metabolic diseases and the role of exercise

Macrophage polarization: implications on metabolic diseases and the role of exercise

Author Sanches Silveira, Loreana Google Scholar
Mello Antunes, Barbara de Moura Google Scholar
Araujo Minari, Andre Luis Autor UNIFESP Google Scholar
Thomatieli dos Santos, Ronaldo Vagner Autor UNIFESP Google Scholar
Rosa Neto, Jose Cesar Google Scholar
Lira, Fabio Santos Google Scholar
Abstract Macrophages are cells of the innate immune response that trigger inflammation resolution. The phenotype of "classically activated macrophages" (M1) has anti-tumoricidal and anti-bactericidal activities. On the other hand, "alternatively activated macrophages" (M2) are involved in tissue remodeling and immunomodulatory functions. The change in the polarization of macrophages varies according to the diversity of cytokines present in the microenvironment or by the stimuli of an antigen. It involves such factors as interferon-regulatory factors, peroxisome proliferator-activated receptors (PPARs), hypoxia-inducible factors (HIFs), and signal transducers and activators of transcription (STATs). Switching the phenotype of macrophages can help attenuate the development of an inflammatory disease. Exercise can promote alterations in the number of innate immune cells and stimulates phagocytic function. Chronic exercise seems to inhibit macrophage infiltration into adipose tissue by attenuating the expression of F4/80 mRNA. Furthermore, exercise may also increase the expression of M2 markers and reduce TNF-alpha and TLR4 mRNA expression, which activates the inflammatory pathway of NF-kappa B. Chronic exercise reduces beta 2-adrenergic receptors in monocytes and macrophages by modulating TLR4 signaling as well as suppressing IL-12 production, a stimulator of interferon.. In this review, we discuss macrophage polarization in metabolic diseases and how exercise can modulate macrophage plasticity.
Keywords Macrophages
Immune System
Inflammation
Exercise
Transcriptional FactorAdipose-Tissue Inflammation
Proliferator-Activated Receptors
Human Skeletal-Muscle
Fatty Liver-Disease
Insulin-Resistance
Ppar-Gamma
Alternative Activation
Lengthening Contractions
Phenotypic Switch
Immune Activation
Language English
Sponsor FAPESP [2014/01246-6, 2014/08003-1, 2013/09367-4, 2013/25310-2]
Grant number FAPESP: 2014/01246-6
FAPESP: 2014/08003-1
FAPESP: 2013/09367-4
FAPESP: 2013/25310-2
Date 2016
Published in Critical Reviews In Eukaryotic Gene Expression. Danbury, v. 26, n. 2, p. 115-132, 2016.
ISSN 1045-4403 (Sherpa/Romeo, impact factor)
Publisher Consel Brasil Oftalmologia
Extent 115-132
Origin http://dx.doi.org/10.1615/CritRevEukaryotGeneExpr.2016015920
Access rights Closed access
Type Article
Web of Science ID WOS:000380778100002
URI http://repositorio.unifesp.br/handle/11600/49441

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