A sweet spot for macrophages: Focusing on polarization

Yang, Depeng; Yang, Lijun; Cai, Jialing; Hu, Xibo; Li, Huaxin; Zhang, Xiaoqing; Zhang, Xiaohan; Chen, Xinghe; Dong, Haiyang; Nie, Huan; Li, Yu

doi:10.1016/j.phrs.2021.105576

Cited by 38 publications

(21 citation statements)

References 233 publications

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“…M1 macrophages, considered as a proinflammatory phenotype, are induced by Th1 cytokines, such as IFN- γ , TNF- α , and lipopolysaccharide (LPS), and tend to produce proinflammatory mediators, including IL, TNF, IFN, inducible nitric oxide synthase (iNOS), and reactive oxygen species (ROS) [ 37 ]. It is commonly believed that M1 macrophages have antimicrobial and antitumoral activity and can mediate ROS-induced tissue damage and impair tissue regeneration.…”

Section: Macrophage Polarization and Osteoporosismentioning

confidence: 99%

Insights into the Role of Macrophage Polarization in the Pathogenesis of Osteoporosis

Wang

Liu

et al. 2022

Oxidative Medicine and Cellular Longevity

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Millions of people worldwide suffer from osteoporosis, which causes bone fragility and increases the risk of fractures. Osteoporosis is closely related to the inhibition of osteogenesis and the enhancement of osteoclastogenesis. In addition, chronic inflammation and macrophage polarization may contribute to osteoporosis as well. Macrophages, crucial to inflammatory responses, display different phenotypes under the control of microenvironment. There are two major phenotypes, classically activated macrophages (M1) and alternatively activated macrophages (M2). Generally, M1 macrophages mainly lead to bone resorption, while M2 macrophages result in osteogenesis. M1/M2 ratio reflects the “fluid” state of macrophage polarization, and the imbalance of M1/M2 ratio may cause disease such as osteoporosis. Additionally, antioxidant drugs, such as melatonin, are applied to change the state of macrophage polarization and to treat osteoporosis. In this review, we introduce the mechanisms of macrophage polarization-mediated bone resorption and bone formation and the contribution to the clinical strategies of osteoporosis treatment.

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Section: Macrophage Polarization and Osteoporosismentioning

confidence: 99%

Insights into the Role of Macrophage Polarization in the Pathogenesis of Osteoporosis

Wang

Liu

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…We further explored the role of CLPM in reversing the biofilminduced immunosuppression. Macrophages are the first line of defense [47] against bacterial invasion in the innate immune system and exhibit high plasticity [48,49] to polarize in different phenotypes depending on the surrounding microenvironment, such as lactate level. Biofilm supernatant without lactate makes macrophages polarize to proinflammatory phenotype (M1), while lactate coerces the polarization of macrophages into the anti-inflammatory phenotype (M2) (Figure S14, Supporting Information), attenuating the bactericidal effect to lead to the immune escape of pathogens.…”

Section: Effects Of Clpm On Macrophage Polarizationmentioning

confidence: 99%

The Self‐Adaptive Nanosystem for Implant‐Related Infections Theranostics via Phase‐Change Driven Anti‐Biofilm and the Enhancement of Immune Memory

Xiao

Yin

et al. 2023

Adv Funct Materials

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Implant‐related infections (IRIs), characterized by the formation of bacterial biofilms and immunosuppressive microenvironment, are a common but tricky clinical issue. In this study, a self‐adaptive theranostics nanosystem is designed based on phase change material (PCM) for IRIs therapy, which can monitor the severity of infection in real time and automatically provide the most appropriate treatment on demand. The nanosystem called CaAlg/LOD/POD@MNO/FAs (CLPM) is made of the fatty acids (FAs) core with dissolved minocycline (MNO) and the calcium alginate (CaAlg) shell with an immobilized lactate oxidase/pyruvate oxidase (LOD/POD) enzyme‐linked system. When the level of infection is mild (wound temperature < 39 °C), the CLPMs perform a bacteriostatic function by slowly releasing MNO from the solid‐phase FAs core. When the infection deteriorates (wound temperature > 39 °C), the solid‐to‐liquid phase change of FAs not only enables a rapid release of MNO but also disrupts the mechanical strength of the biofilm skeleton doped with CLPM, performing a bactericidal function. In addition, CLPM can reduce the accumulation of bacteria‐derived lactate to address lactate‐induced immunosuppression and enhance immune memory response, thereby inhibiting infection recurrence.

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“…Abnormal and/or prolonged polarization into the M1 phenotype may exaggerate the tissue injury and preclude recovery from inflammation. In the course of diabetes, several stimuli increase the M1 phenotype predominance, thus promoting inflammation, oxidative stress and target tissue injuries [ 113 ]. Induction of phenotype transition from M1 to M2 has been postulated for a long time as one of the promising methods in the treatment of inflammatory or malignant diseases.…”

Section: Glp1r Agonists As Antioxidative and Anti-inflammatory Agents In Other Tissues And Organsmentioning

confidence: 99%

Inflammation and Oxidative Stress in Diabetic Kidney Disease: The Targets for SGLT2 Inhibitors and GLP-1 Receptor Agonists

Winiarska

Knysak

Nabrdalik

et al. 2021

IJMS

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The incidence of type 2 diabetes (T2D) has been increasing worldwide, and diabetic kidney disease (DKD) remains one of the leading long-term complications of T2D. Several lines of evidence indicate that glucose-lowering agents prevent the onset and progression of DKD in its early stages but are of limited efficacy in later stages of DKD. However, sodium-glucose cotransporter-2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor (GLP-1R) antagonists were shown to exert nephroprotective effects in patients with established DKD, i.e., those who had a reduced glomerular filtration rate. These effects cannot be solely attributed to the improved metabolic control of diabetes. In our review, we attempted to discuss the interactions of both groups of agents with inflammation and oxidative stress—the key pathways contributing to organ damage in the course of diabetes. SGLT2i and GLP-1R antagonists attenuate inflammation and oxidative stress in experimental in vitro and in vivo models of DKD in several ways. In addition, we have described experiments showing the same protective mechanisms as found in DKD in non-diabetic kidney injury models as well as in some tissues and organs other than the kidney. The interaction between both drug groups, inflammation and oxidative stress appears to have a universal mechanism of organ protection in diabetes and other diseases.

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A sweet spot for macrophages: Focusing on polarization

Cited by 38 publications

References 233 publications

Insights into the Role of Macrophage Polarization in the Pathogenesis of Osteoporosis

Insights into the Role of Macrophage Polarization in the Pathogenesis of Osteoporosis

The Self‐Adaptive Nanosystem for Implant‐Related Infections Theranostics via Phase‐Change Driven Anti‐Biofilm and the Enhancement of Immune Memory

Inflammation and Oxidative Stress in Diabetic Kidney Disease: The Targets for SGLT2 Inhibitors and GLP-1 Receptor Agonists

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