scholarly journals The Reactive Oxygen Species in Macrophage Polarization: Reflecting Its Dual Role in Progression and Treatment of Human Diseases

2016 ◽  
Vol 2016 ◽  
pp. 1-16 ◽  
Author(s):  
Hor-Yue Tan ◽  
Ning Wang ◽  
Sha Li ◽  
Ming Hong ◽  
Xuanbin Wang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Macrophage Polarization ◽  
Human Diseases ◽  
Environmental Cues ◽  
Oxygen Species ◽  
M2 Macrophages ◽  
M1 Macrophages ◽  
M1 Phenotype ◽  
Full Activation ◽  
M1 And M2 Macrophages

High heterogeneity of macrophage is associated with its functions in polarization to different functional phenotypes depending on environmental cues. Macrophages remain in balanced state in healthy subject and thus macrophage polarization may be crucial in determining the tissue fate. The two distinct populations, classically M1 and alternatively M2 activated, representing the opposing ends of the full activation spectrum, have been extensively studied for their associations with several disease progressions. Accumulating evidences have postulated that the redox signalling has implication in macrophage polarization and the key roles of M1 and M2 macrophages in tissue environment have provided the clue for the reasons of ROS abundance in certain phenotype. M1 macrophages majorly clearing the pathogens and ROS may be crucial for the regulation of M1 phenotype, whereas M2 macrophages resolve inflammation which favours oxidative metabolism. Therefore how ROS play its role in maintaining the homeostatic functions of macrophage and in particular macrophage polarization will be reviewed here. We also review the biology of macrophage polarization and the disturbance of M1/M2 balance in human diseases. The potential therapeutic opportunities targeting ROS will also be discussed, hoping to provide insights for development of target-specific delivery system or immunomodulatory antioxidant for the treatment of ROS-related diseases.

Abstract 520: High-density Lipoprotein Inhibits Human M1 Macrophage Polarisation through the Redistribution of Caveolin-1

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Man K Lee ◽  
Xiao-Lei Moore ◽  
Yi Fu ◽  
Annas Al-sharea ◽  
Dragana Dragoljeic ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cholesterol Efflux ◽  
Human Macrophage ◽  
Ros Production ◽  
Oxygen Species ◽  
M1 Macrophages ◽  
Macrophage Polarisation ◽  
Caveolin 1 ◽  
M1 Phenotype ◽  
M2 Phenotype

Macrophages play a critical role in the development and progression of atherosclerosis. Depending on their surrounding milieu, macrophages can adopt a wide range of functional phenotypes; pro-inflammatory (M1) and pro-resolving (M2). HDL has many cardio-protective properties including potent anti-inflammatory effects, largely through the removal of cholesterol from cells. It is currently not known if this extends to influencing human macrophage phenotypes. Thus, we aimed to investigate the effect of HDL on human macrophage polarisation. Human blood monocyte-derived macrophages were induced to either an M1-phenotype by incubation with LPS and IFN-γ or to an M2-phenotype with IL-4. Macrophages were differentiated in the presence or absence of human HDL and their phenotypes were characterised using cell surface markers, reactive oxygen species (ROS) production by flow cytometry, and mRNA expression by real-time PCR. Downstream signalling pathways were also explored. We discovered that HDL inhibited the induction to M1 as evidenced by a decrease in cell surface marker expression; CD192 and CD64. This was accompanied by a decreased expression of M1-associated inflammatory genes TNF-α, IL-6 and MCP-1. However, HDL had no effect on induction to the M2 phenotype. Similarly, methyl-beta-cyclodextrin (MβCD), a non-specific cholesterol acceptor was also able to suppress M1 induction suggesting cholesterol efflux is important in this process. Further we found that HDL decreased membrane caveolin-1 in M1 macrophages and redistributed it intracellularly. The requirement of caveolin-1 was revealed as bone marrow-derived macrophages from Cav-1-/- mice continued to differentiate into M1 despite the addition of HDL. Moreover, we demonstrated a decrease in STAT3 and ERK1/2 phosphorylation in M1 macrophages treated with HDL, suggesting cholesterol efflux inhibits the STAT3s and MAPKs during induction to the M1 phenotype. Finally, we found that HDL also inhibited M1 function; with reduced reactive oxygen species (ROS) production. We provide evidence that HDL reduces macrophage induction to the inflammatory M1 phenotype, but not M2, via cellular redistribution of caveolin-1 and inactivation of STAT3 and ERK1/2 signalling pathway.

Immunohistochemical Study of M1 and M2 Macrophages Population in Chronic Villitis of the Placenta

2019 ◽  
Vol 152 (Supplement_1) ◽  
pp. S102-S102
Author(s):  
Erika Egal ◽  
Natalia de Magalhães Rodrigues ◽  
Fernanda Mariano ◽  
Reydson Souza ◽  
Joao Scarini ◽  
...  
Keyword(s):  
Tissue Repair ◽  
Etiologic Agent ◽  
Unknown Etiology ◽  
M2 Macrophages ◽  
M1 Macrophages ◽  
Effector Cells ◽  
Intervillous Space ◽  
M1 Phenotype ◽  
Chronic Villitis ◽  
M1 And M2 Macrophages

Abstract Introduction Villitis is characterized by the presence of inflammatory infiltrate (CD8 lymphocyte) in the placental villous and is classified as to the etiology in known and unknown. In most cases, villitis is idiopathic (villitis of unknown etiology [VUE]) because no microorganisms are evident and there are no maternal symptoms or signs. It has recently been proposed that pregnancy is, in fact, an active and highly regulated immune process in which macrophages play an important role. Macrophages may present with M1 phenotype, important effector cells, or M2 phenotype, capable of suppressing the function of M1 macrophages and influencing immunoregulation and tissue repair. CD68 antibody recognizes macrophages M1 and M2, whereas CD11c and CD163 antibodies are specific for the identification only of M1 and M2 macrophages, respectively. The objective of our study is to characterize in human placentas in the subpopulation of M1 and M2 macrophages in VUE. Methods Sixteen cases of chronic villitis (all without an identifiable etiologic agent) and three control placentas were examined using immunohistochemistry with antibodies for CD68, CD11c, CD163, and CD3. Results CD68 and CD163 were present in all cases in the normal areas. CD68, CD163, and CD11c were present in the villous stroma and in the intervillous space in the inflamed areas. The percentage of CD68-positive macrophages was higher than CD163- and CD11c-positive macrophages in all specimens studied. A total increase of CD68, CD163, and CD11c with the predominance of CD11c over CD163 in the inflamed areas was observed. Conclusion The predominance of M1 macrophages (CD11c) in the inflamed areas suggests the influence of these cells in the pathogenesis VUE. The higher amount of M2 (CD163) in the inflamed villous compared to normal areas suggests a possible immunoregulatory mechanism of the inflammatory process in VUE.

scholarly journals Effect of Propofol on the Production of Inflammatory Cytokines by Human Polarized Macrophages

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Tsukasa Kochiyama ◽  
Xiaojia Li ◽  
Hitoshi Nakayama ◽  
Madoka Kage ◽  
Yui Yamane ◽  
...  
Keyword(s):  
Nuclear Translocation ◽  
Inflammatory Responses ◽  
Macrophage Polarization ◽  
Signal Transduction Pathway ◽  
Induce Polarization ◽  
Human Macrophage ◽  
Related Factor ◽  
M2 Macrophages ◽  
M1 Macrophages ◽  
Inflammatory Processes

Macrophages are key immune system cells involved in inflammatory processes. Classically activated (M1) macrophages are characterized by strong antimicrobicidal properties, whereas alternatively activated (M2) macrophages are involved in wound healing. Severe inflammation can induce postoperative complications during the perioperative period. Invasive surgical procedures induce polarization to M1 macrophages and associated complications. As perioperative management, it is an important strategy to regulate polarization and functions of macrophages during inflammatory processes. Although propofol has been found to exhibit anti-inflammatory activities in monocytes and macrophages, it is unclear whether propofol regulates the functions of M1 and M2 macrophages during inflammatory processes. This study therefore investigated the effects of propofol on human macrophage polarization. During M1 polarization, propofol suppressed the production of IL-6 and IL-1β but did not affect TNF-α production. In contrast, propofol did not affect the gene expression of M2 markers, such as IL-10, TGF-β, and CD206, during M2 polarization. Propofol was similar to the GABAA agonist muscimol in inducing nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2) and inhibiting IL-6 and IL-1β, but not TNF-α, production. Knockdown of Nrf2 using siRNA significantly reduced the effect of propofol on IL-6 and IL-1β production. These results suggest that propofol prevents inflammatory responses during polarization of human M1 macrophages by suppressing the expression of IL-6 and IL-1β through the GABAA receptor and the Nrf2-mediated signal transduction pathway.

Deconvoluting the role of reactive oxygen species and autophagy in human diseases

2013 ◽  
Vol 65 ◽  
pp. 402-410 ◽  
Author(s):  
Xin Wen ◽  
Jinming Wu ◽  
Fengtian Wang ◽  
Bo Liu ◽  
Canhua Huang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Human Diseases ◽  
Oxygen Species

scholarly journals The Language of Reactive Oxygen Species Signaling in Plants

2012 ◽  
Vol 2012 ◽  
pp. 1-22 ◽  
Author(s):  
Soumen Bhattacharjee
Keyword(s):  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Signal Transduction ◽  
Lipid Peroxidation ◽  
Reactive Oxygen ◽  
Environmental Cues ◽  
Oxygen Species ◽  
Lipid Peroxidation Products ◽  
Expression Of Genes ◽  
Regulated Gene Expression

Reactive oxygen species (ROS) are astonishingly versatile molecular species and radicals that are poised at the core of a sophisticated network of signaling pathways of plants and act as core regulator of cell physiology and cellular responses to environment. ROS are continuously generated in plants as an inevitable consequence of redox cascades of aerobic metabolism. In one hand, plants are surfeited with the mechanism to combat reactive oxygen species, in other circumstances, plants appear to purposefully generate (oxidative burst) and exploit ROS or ROS-induced secondary breakdown products for the regulation of almost every aspect of plant biology, from perception of environmental cues to gene expression. The molecular language associated with ROS-mediated signal transduction, leading to modulation in gene expression to be one of the specific early stress response in the acclamatory performance of the plant. They may even act as “second messenger” modulating the activities of specific proteins or expression of genes by changing redox balance of the cell. The network of redox signals orchestrates metabolism for regulating energy production to utilization, interfering with primary signaling agents (hormones) to respond to changing environmental cues at every stage of plant development. The oxidative lipid peroxidation products and the resulting generated products thereof (associated with stress and senescence) also represent “biological signals,” which do not require preceding activation of genes. Unlike ROS-induced expression of genes, these lipid peroxidation products produce nonspecific response to a large variety of environmental stresses. The present review explores the specific and nonspecific signaling language of reactive oxygen species in plant acclamatory defense processes, controlled cell death, and development. Special emphasis is given to ROS and redox-regulated gene expression and the role of redox-sensitive proteins in signal transduction event. It also describes the emerging complexity of apparently contradictory roles that ROS play in cellular physiology to ascertain their position in the life of the plant.

M1 and M2 macrophages within human carotid plaques express different NPY receptors: are they involved in macrophage polarization?

2017 ◽  
Vol 263 ◽  
pp. e124
Author(s):  
Rita Businaro ◽  
Ilia Elenkov ◽  
Mariangela Corsi ◽  
Tania Di Raimo ◽  
Elisa Maggi ◽  
...  
Keyword(s):  
Macrophage Polarization ◽  
M2 Macrophages ◽  
Carotid Plaques ◽  
Npy Receptors ◽  
M1 And M2 Macrophages ◽  
Human Carotid

scholarly journals Abnormal Macrophage Polarization in Patients with Myelodysplastic Syndrome

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Gaochao Zhang ◽  
Liyan Yang ◽  
Yu Han ◽  
Haiyue Niu ◽  
Li Yan ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Myelodysplastic Syndrome ◽  
Macrophage Polarization ◽  
Control Group ◽  
M2 Macrophages ◽  
M1 Macrophages ◽  
Tnf Α ◽  
Bone Marrow Microenvironments ◽  
Medical University

Background. This study is aimed at assessing the subsets of bone marrow macrophages in patients with myelodysplastic syndrome (MDS) and exploring the role of macrophages in the pathogenesis of MDS. Methods. Thirty-eight newly diagnosed MDS patients were enrolled in the Department of Hematology of General Hospital of Tianjin Medical University from June 2015 to June 2016. Bone marrow monocytes and macrophage subsets (M1/M2) were detected in patients with MDS and normal controls by flow cytometry. M1 macrophages were cultured in vitro, and the expression of IL-1β and TNF-α mRNA was measured using real-time polymerase chain reaction. Results. Compared with the normal control group, the proportion of bone marrow monocytes was higher ( 2.11 ± 0.93 % vs. 3.66 ± 3.38 % ), and the mean fluorescence intensity of surface molecule CD14 was lower in the higher-risk (HR) MDS group ( 639.05 ± 359.78 vs. 458.26 ± 306.72 , p < 0.05 ). The ratio of M2 macrophages to monocytes was higher in patients with HR-MDS ( 1.82 ± 2.47 % vs. 3.93 ± 3.81 % , p < 0.05 ). The ratio of M1 to M2 macrophages was lower in the HR-MDS group ( 3.50 ± 3.22 vs. 1.80 ± 0.88 , p < 0.05 ). The expression of IL-1β and TNF-α mRNA in M1 macrophages was significantly lower in the MDS group ( p < 0.05 ). Conclusions. Patients with MDS had abnormal macrophage polarization, which may be involved in the alteration of bone marrow microenvironments.

scholarly journals Phenotype and function of macrophage polarization in monocrotaline-induced pulmonary arterial hypertension rat model

2021 ◽  
Author(s):  
Yong Fan ◽  
Yanjie Hao ◽  
Dai Gao ◽  
Lan Gao ◽  
Guangtao Li ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Lung Tissue ◽  
Rat Model ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
M2 Macrophages ◽  
M1 Macrophages ◽  
Pulmonary Arterial

Pulmonary arterial hypertension (PAH) is a fatal disease characterized by vascular remodeling and chronic inflammation. Macrophages are the key orchestrators of inflammatory and repair responses, and have been demonstrated to be vital in the pathogenesis of PAH. However, specific phenotype of macrophage polarization (M1 & M2 macrophage) in the development of PAH and the underlying mechanisms how they work are still largely unclear. A rat model of monocrotaline (MCT) induced PAH was used. Hemodynamic analysis and histopathological experiments were conducted at day 3, 7, 14, 21 and 28, respectively. In PAH rat lung tissue, confocal microscopic images showed that CD68+NOS2+ M1-like macrophages were remarkably infiltrated on early stage, but dramatically decreased in mid-late stage. Meanwhile, CD68+CD206+ M2-like macrophages in lung tissue accumulated gradually since day 7 to day 28, and the relative ratio of M2/M1 macrophage increased over time. Results detected by western blot and immunohistochemistry were consistent. Further vitro functional studies revealed the possible mechanism involved in this pathophysiological process. By using Transwell co-culture system, it was found that M1 macrophages induced endothelial cell apoptosis, while M2 macrophages significantly promoted proliferation of both endothelial cell and smooth muscle cell. These data preliminarily demonstrated a temporal dynamic change of macrophage M1/M2 polarization status in the development of experimental PAH. M1 macrophages participated in the initial stage of inflammation by accelerating apoptosis of endothelial cell, while M2 macrophages predominated in the reparative stage of inflammation and the followed stage of aberrant tissue remodeling.

scholarly journals Schistosome eggs stimulate reactive oxygen species production to enhance M2 macrophage differentiation and promote hepatic pathology in schistosomiasis

2021 ◽  
Vol 15 (8) ◽  
pp. e0009696
Author(s):  
Yanxiong Yu ◽  
Junling Wang ◽  
Xiaohong Wang ◽  
Pan Gu ◽  
Zhigang Lei ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Schistosomiasis Japonica ◽  
Health Concern ◽  
M2 Macrophage ◽  
Ros Production ◽  
Oxygen Species ◽  
M2 Macrophages ◽  
Macrophage Differentiation ◽  
Hepatic Pathology

Schistosomiasis is a neglected tropical disease of public health concern. The most devastating pathology in schistosomiasis japonica and mansoni is mainly attributed to the egg-induced granulomatous response and secondary fibrosis in host liver, which may lead to portal hypertension or even death of the host. Schistosome eggs induce M2 macrophages-rich granulomas and these M2 macrophages play critical roles in the maintenance of granuloma and subsequent fibrosis. Reactive oxygen species (ROS), which are highly produced by stimulated macrophages during infection and necessary for the differentiation of M2 macrophages, are massively distributed around deposited eggs in the liver. However, whether ROS are induced by schistosome eggs to subsequently promote M2 macrophage differentiation, and the possible underlying mechanisms as well, remain to be clarified during S. japonicum infection. Herein, we observed that extensive expression of ROS in the liver of S. japonicum-infected mice. Injection of ROS inhibitor in infected mice resulted in reduced hepatic granulomatous responses and fibrosis. Further investigations revealed that inhibition of ROS production in S. japonicum-infected mice reduces the differentiation of M2, accompanied by increased M1 macrophage differentiation. Finally, we proved that S. japonicum egg antigens (SEA) induce a high level of ROS production via both nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) and mitochondria in macrophages. Our study may help to better understand the mechanism of schistosomiasis japonica-induced hepatic pathology and contribute to the development of potential therapeutic strategies by interfering with ROS production.

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