Feruloylated arabinoxylan from wheat bran inhibited M1-macrophage activation and enhanced M2-macrophage polarization

2021 ◽  
Author(s):  
Jing Wang ◽  
Junying Bai ◽  
Yu Wang ◽  
Kuiliang Zhang ◽  
Yan Li ◽  
...  
Keyword(s):  
Wheat Bran ◽  
Macrophage Activation ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
M1 Macrophage ◽  
M2 Macrophage Polarization

scholarly journals Effect of Platelet-Rich Plasma on M1/M2 Macrophage Polarization

2021 ◽  
Vol 22 (5) ◽  
pp. 2336
Author(s):  
Ryoka Uchiyama ◽  
Eriko Toyoda ◽  
Miki Maehara ◽  
Shiho Wasai ◽  
Haruka Omura ◽  
...  
Keyword(s):  
Culture Media ◽  
Platelet Rich Plasma ◽  
Point Of Care ◽  
Macrophage Polarization ◽  
Osteoarthritis Of The Knee ◽  
M2 Macrophage ◽  
Related Factors ◽  
Humoral Factors ◽  
M1 Macrophage ◽  
M2 Macrophage Polarization

Osteoarthritis of the knee (OAK) is a chronic degenerative disease and progresses with an imbalance of cytokines and macrophages in the joint. Studies regarding the use of platelet-rich plasma (PRP) as a point-of-care treatment for OAK have reported on its effect on tissue repair and suppression of inflammation but few have reported on its effect on macrophages and macrophage polarization. Based on our clinical experience with two types of PRP kits Cellaid Serum Collection Set P type kit (leukocyte-poor-PRP) and an Autologous Protein Solution kit (APS leukocyte-rich-PRP), we investigated the concentrations of humoral factors in PRPs prepared from the two kits and the effect of humoral factors on macrophage phenotypes. We found that the concentrations of cell components and humoral factors differed between PRPs purified using the two kits; APS had a higher concentration of M1 and M2 macrophage related factors. The addition of PRP supernatants to the culture media of monocyte-derived macrophages and M1 polarized macrophages revealed that PRPs suppressed M1 macrophage polarization and promoted M2 macrophage polarization. This research is the first to report the effect of PRPs purified using commercial kits on macrophage polarization.

scholarly journals MiR-520a-3p Inhibited Macrophage Polarization and Promoted the Development of Atherosclerosis via Targeting UVRAG in Apolipoprotein E Knockout Mice

2021 ◽  
Vol 7 ◽  
Author(s):  
Jing Rui Qi ◽  
Dian Ru Zhao ◽  
Li Zhao ◽  
Fan Luo ◽  
Mei Yang
Keyword(s):  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Treatment Target ◽  
Vessel Disease ◽  
Novel Treatment ◽  
M1 Macrophage ◽  
Apolipoprotein E Knockout Mice ◽  
The World ◽  
M2 Macrophage Polarization

Atherosclerosis (AS), a kind of chronic inflammatory blood vessel disease, is a main cause of cardiovascular disease, which is a leading cause of mortality around the world. Accumulation of macrophages induced by inflammation contributes to AS development. It has been indicated that microRNAs (miRNAs) are involved in the process of AS. However, the pathway and gene miRNAs targeting are poorly understood. Here we reported that miR-520a-3p was increased in mice with AS and silencing of miR-520a-3p attenuated AS process. Furthermore, inhibition of miR-520a-3p increased the expression of α-SMA and collagen. In addition, miR-520a-3p silencing inhibited the expression of M1 macrophage polarization markers and pro-inflammatory genes and promoted the M2 macrophage polarization. What’s more, forced expression of miR-520a-3p diminished IL4/IL13 induced macrophage autophagy via targeting UVRAG. Collectively, our study reveals the role of miR-520a-3p in macrophage polarization and suggests the potential of miRNA as a novel treatment target of AS.

scholarly journals Modulation of M2 macrophage polarization by the crosstalk between Stat6 and Trim24

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Tao Yu ◽  
Shucheng Gan ◽  
Qingchen Zhu ◽  
Dongfang Dai ◽  
Ni Li ◽  
...  
Keyword(s):  
Immune Responses ◽  
Macrophage Activation ◽  
Regulatory Mechanism ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Creb Binding Protein ◽  
Human Macrophages ◽  
M2 Polarization ◽  
M2 Macrophage Polarization ◽  
Negative Regulatory Mechanism

Abstract Stat6 is known to drive macrophage M2 polarization. However, how macrophage polarization is fine-tuned by Stat6 is poorly understood. Here, we find that Lys383 of Stat6 is acetylated by the acetyltransferase CREB-binding protein (CBP) during macrophage activation to suppress macrophage M2 polarization. Mechanistically, Trim24, a CBP-associated E3 ligase, promotes Stat6 acetylation by catalyzing CBP ubiquitination at Lys119 to facilitate the recruitment of CBP to Stat6. Loss of Trim24 inhibits Stat6 acetylation and thus promotes M2 polarization in both mouse and human macrophages, potentially compromising antitumor immune responses. By contrast, Stat6 mediates the suppression of TRIM24 expression in M2 macrophages to contribute to the induction of an immunosuppressive tumor niche. Taken together, our findings establish Stat6 acetylation as an essential negative regulatory mechanism that curtails macrophage M2 polarization.

Ginsenoside Rg1 Ameliorated Colitis by Regulating the Homeostasis of M1/M2 Macrophage Polarization and Intestinal Flora

2021 ◽  
Author(s):  
Jian Long ◽  
Xue-Ke Liu ◽  
Zeng-Ping Kang ◽  
Meng-Xue Wang ◽  
Hai-Mei Zhao ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Macrophage Activation ◽  
Macrophage Polarization ◽  
Intestinal Flora ◽  
M2 Macrophage ◽  
Ginsenoside Rg1 ◽  
Tnf Α ◽  
M2 Macrophage Polarization ◽  
Rhoa Signaling

Abstract Background: Aberrant M1/M2 macrophage polarization and intestinal flora disruption are involved in the pathological processes associated with ulcerative colitis (UC). Ginsenoside Rg1 has good immunomodulatory and anti-inflammatory effects and is effective in treating UC of humans and animals. However, it is unclear how ginsenoside Rg1 regulate the homeostasis of M1/M2 macrophage polarization and intestinal flora.Methods: BALB/c mice were randomly divided into 4 groups: Control, DSS, DSS+Rg1, DSS+Y27632 groups. In this study, experiment colitis was induced in BALB/c mice using sodium dextran sulfate (DSS). Mice of DSS+Rg1, DSS+Y27632 groups were treated respectively with ginsenoside Rg1 and Rock inhibitor Y27632 for 14 consecutive days. On day 21, all mice were sacrificed. Histopathological analysis of the colon tissues was performed by Hematoxylin Eosin sinning. Cytokines (IL-6, IL-33, CCL-2, TNF-α, IL-4 and IL-10) were detected by Elisa. Flow cytometry was used to analyse macrophage activation and M1/M2 macrophage polarisation. Western blotting were applied to detect the levels of Macrophage polarization-associated protein (Arg-1, MIF-1, PIM-1, TLR2) and Nogo-B/RhoA signaling molecules (Rock1, RhoA and Nogo-B). The fecal microbial populations were analyzed using 16S gene sequencing. Results: After ginsenoside Rg1 and Y27632 treatment, the changes of body weight, colon length, colonic weight index and colonic mucosal injury of colitis mice were effectively improved, accompanied by less ulcer formation and inflammatory cell infiltration, lower levels of pro-inflammatory cytokines (IL-6, IL-33, CCL-2, TNF-α) and higher anti-inflammatory cytokines (IL-4 and IL-10). Importantly, the percentage of CD11b+F4/80+, CD11b+F4/80+Tim-1+, CD11b+F4/80+TLR4+, and CD11b+F4/80+iNOS+ cells and the expression levels of MIF-1 and PIM-1 proteins were down-regulated significantly after ginsenoside Rg1 and Y27632 treatment, and CD11b+F4/80+CD206+ and CD11b+F4/80+CD163+ cells and Arg-1 up-regulated significantly. Intestinal flora composition were effectively improved after administration of ginsenoside Rg1. The Nogo-B/RchoA signaling pathway were obviously inhibited after ginsenoside Rg1 and Y27632 treatment, and the levels of Rock1, RhoA and Nogo-B proteins were significantly reduced. Conclusions: Ginsenoside Rg1 has the protective effect on UC by inhibiting macrophage activation, restoring the balance of M1/M2 macrophage polarization, and improving intestinal flora composition, associated with inhibition of the Nogo-B/RhoA signaling pathway.

scholarly journals A Benzenediamine Analog FC-99 Drives M2 Macrophage Polarization and Alleviates Lipopolysaccharide- (LPS-) Induced Liver Injury

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Wei Gong ◽  
Haiyan Zhu ◽  
Li Lu ◽  
Yayi Hou ◽  
Huan Dou
Keyword(s):  
Liver Injury ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
M1 Macrophage ◽  
M2 Macrophage Polarization ◽  
Underlying Mechanisms ◽  
Sirna Knockdown ◽  
Lower Expression ◽  
Alternatively Activated

Macrophages have variable functional phenotypes, high diversity, and plasticity and are involved in the pathogenesis of sepsis-induced liver injury. Alteration of macrophage polarization through activated (M1) macrophage to alternatively activated (M2) macrophage has emerged as a potential therapeutic strategy. This study was designed to explore the effect of a benzenediamine analog FC-99 on macrophage polarization in vitro and lipopolysaccharide- (LPS-) induced liver injury followed by the underlying mechanisms. For in vitro experiments, FC-99 inhibited M1-related macrophage factors and promoted M2-related markers induced by IL-4 in the mouse macrophage cell line RAW264.7. Moreover, FC-99-induced macrophages polarized to M2 phenotype which could be repressed by a PPAR-γ inhibitor but not STAT6 siRNA knockdown, indicating FC-99-induced M2 macrophage polarization through PPAR-γ rather than STAT6 signal. In LPS-induced septic mice, FC-99 pretreated mice displayed lower expression of M1 markers together with the increased M2 marker CD206 and improvement of liver injury. These findings illustrated that FC-99 could promote M2 macrophage polarization via PPAR-γ signaling and seemed to be a potential therapeutic candidate for inflammatory liver injury.

scholarly journals MiR-98-5p expression inhibits polarization of macrophages to an M2 phenotype by targeting Trib1 in inflammatory bowel disease

2020 ◽  
Author(s):  
Yunhua Peng ◽  
Qingyuan Wang ◽  
Wei Yang ◽  
Qiqi Yang ◽  
Ynani Pei ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Macrophage Polarization ◽  
Luciferase Reporter ◽  
Marker Genes ◽  
M2 Macrophage ◽  
M1 Macrophage ◽  
Inflammatory Bowel ◽  
M2 Macrophage Polarization ◽  
M2 Phenotype

Herein, we unfolded miR-98-5p mechanism in inflammatory bowel disease (IBD). IBD mouse model was established. The severity of colitis was assessed daily using the disease activity index (DAI). Murine peritoneal macrophages were stimulated by lipopolysaccharide (LPS). MiR-98-5p, tribbles homolog 1 (Trib1), M1 and M2 macrophage marker genes mRNA expression was analyzed. The relationship between miR-98-5p and Trib1 was explored using a luciferase reporter assay. The strategy of loss-of-function was used to explore the mechanism of miR-98-5p in macrophage polarization, inflammation and IBD. The results revealed that IBD mice had higher DAI index and miR-98-5p expression when compared to the Sham group. MiR-98-5p and Trib1 displayed a targeted regulation relationship. Knockdown of miR-98-5p transformed LPS-induced M1 macrophage polarization into M2 macrophage polarization and inhibited inflammation via up-regulating Trib1. However, shTrib1 reversed the effects. In vivo experiment, silencing of miR-98-5p, diminished the DAI and promoted M2 macrophage polarization. In conclusion, knockdown of miR-98-5p changed macrophage polarization to the M2 phenotype by increasing Trib1 expression, thereby alleviating IBD symptoms.

scholarly journals Propofol inhibits inflammatory response by regulating the miR-494/ Nrdp1 pathway in ICH mice model

2020 ◽  
Author(s):  
Shudong Liu ◽  
Wenyan Li ◽  
Hui Shi ◽  
Ge Tang ◽  
Jiangwei Zhang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Mice Model ◽  
Immune Disease ◽  
Neuroinflammatory Response ◽  
M1 Macrophage ◽  
M2 Macrophage Polarization ◽  
Neuro Protective Effect ◽  
Proinflammatory Factors

Abstract Background: Propofol is an anesthetic agent with neuro-protective effect in neuronal injury. However, the mechanism of propofol in M1 macrophage polarization following ICH has not been well studied. Ubiquitination mediated M1/M2 macrophage polarization plays important roles in pathogenesis of immune disease. The experiment analyzed anti-inflammatory effects of propofol in macrophages following ICH. Methods: In the experiment, macrophages were administrated with erythrocyte lysates, and then miR-494, Nrdp1 and M1 related markers were analyzed. In addition, brain inflammatory response, brain edema, and neurological functions of ICH mice were also assessed. Results: We found that propofol decreased miR-494 levels while increased Nrdp1 levels in macrophages after ICH. We also demonstrated that miR-494 inhibited Nrdp1 expression by directly binding its 3′-untranslated region. MiR-494 attenuated Nrdp1 levels and downstream proinflammatory factors production. Upregulation of Nrdp1 in macrophages significantly decreased M1 macrophage polarization. Conclusion: Taken together, these results suggest that propofol can attenuate the neuroinflammatory response of macrophages after ICH through regulation of the miR-494/Nrdp1 pathway.

scholarly journals Propofol inhibits inflammatory response by regulating the miR-494/ Nrdp1 pathway in ICH mice model

2020 ◽  
Author(s):  
Hui Shi ◽  
Qijiang Xiong ◽  
Zhongyan Huang ◽  
zhao yang
Keyword(s):  
Inflammatory Response ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Mice Model ◽  
Immune Disease ◽  
Neuroinflammatory Response ◽  
M1 Macrophage ◽  
M2 Macrophage Polarization ◽  
Neuro Protective Effect ◽  
Proinflammatory Factors

Abstract Background: Propofol is an anesthetic agent with neuro-protective effect in neuronal injury. However, the mechanism of propofol in M1 macrophage polarization following ICH has not been well studied. Ubiquitination mediated M1/M2 macrophage polarization plays important roles in pathogenesis of immune disease. The experiment analyzed anti-inflammatory effects of propofol in macrophages following ICH. Methods: In the experiment, macrophages were administrated with erythrocyte lysates, and then miR-494, Nrdp1 and M1 related markers were analyzed. In addition, brain inflammatory response, brain edema, and neurological functions of ICH mice were also assessed. Results: We found that propofol decreased miR-494 levels while increased Nrdp1 levels in macrophages after ICH. We also demonstrated that miR-494 inhibited Nrdp1 expression by directly binding its 3′-untranslated region. MiR-494 attenuated Nrdp1 levels and downstream proinflammatory factors production. Upregulation of Nrdp1 in macrophages significantly decreased M1 macrophage polarization. Conclusion: Taken together, these results suggest that propofol can attenuate the neuroinflammatory response of macrophages after ICH through regulation of the miR-494/Nrdp1 pathway.

scholarly journals The N6-methyladenosine (m6A)-forming enzyme METTL3 facilitates M1 macrophage polarization through the methylation of STAT1 mRNA

2019 ◽  
Vol 317 (4) ◽  
pp. C762-C775 ◽  
Author(s):  
Yihan Liu ◽  
Zhujiang Liu ◽  
Hao Tang ◽  
Yicong Shen ◽  
Ze Gong ◽  
...  
Keyword(s):  
Epigenetic Modification ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
M1 Polarization ◽  
M1 Macrophage ◽  
Mouse Macrophages ◽  
Rna Immunoprecipitation ◽  
M2 Macrophage Polarization ◽  
Plasmid Transfection

Compelling evidence indicates that epigenetic regulations orchestrate dynamic macrophage polarization. N6-methyladenosine (m6A) methylation is the most abundant epigenetic modification of mammalian mRNA, but its role in macrophage polarization is still completely unknown. Here, we show that the m6A-catalytic enzyme methyltransferase like 3 (METTL3) is specifically upregulated following the M1 polarization of mouse macrophages. Furthermore, METTL3 knockdown through siRNA transfection markedly inhibited M1, but enhanced M2, macrophage polarization. Conversely, its overexpression via plasmid transfection greatly facilitated M1, but attenuated M2, macrophage polarization. Further methylated RNA immunoprecipitation and in vitro m6A methylation assays suggested that METTL3 directly methylates mRNA encoding signal transducer and activator of transcription 1 (STAT1), a master transcription factor controlling M1 macrophage polarization, at its coding sequence and 3′-untranslated regions. In addition, METTL3-mediated STAT1 mRNA methylation significantly increased mRNA stability and subsequently upregulated STAT1 expression. In conclusion, METTL3 drives M1 macrophage polarization by directly methylating STAT1 mRNA, potentially serving as an anti-inflammatory target.

scholarly journals Saponin from Periploca forrestii Schltr Mitigates Oxazolone-Induced Atopic Dermatitis via Modulating Macrophage Activation

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Luting Zeng ◽  
Yingqin Liu ◽  
Congcong Xing ◽  
Yijie Huang ◽  
Xin Sun ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Macrophage Activation ◽  
Skin Diseases ◽  
Nuclear Translocation ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Mouse Bone Marrow ◽  
Inflammatory Skin Diseases ◽  
M1 Macrophage

Atopic dermatitis (AD) is a relapsing, acute, and chronic skin disease featured by intractable itching, eczematous skin. Conventional therapies based on immunosuppression such as corticosteroids are associated with multiple adverse reactions. Periploca forrestii Schltr saponin (PFS) was shown to potently inhibit murine arthritis by protecting bone and cartilage injury and suppressing NF-κB activation. However, its therapeutic effect on oxazolone-induced atopic dermatitis (AD) and the underlying mechanisms on macrophage are still unclear. The AD-like dermatitis was induced by repeated oxazolone challenge to the skin of BALB/c mice in vivo. Blood and ears were biochemically or histologically processed. RT-PCR, western blotting, and ELISA were conducted to evaluate the expression of macrophage factors. Mouse bone marrow-derived macrophages (BMDMs) stimulated with lipopolysaccharide (LPS) were used as a model in vitro. PFS treatment inhibited AD-like dermatitis development. PFS downregulated epidermis thickness and cell infiltration, with histological analysis of the skin lesion. PFS alleviated plasma immunoglobulin (Ig) E, IgG2a, and IgG1 levels. PFS downregulated the expression of M1 macrophage factors, tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, monocyte chemotactic protein-1 (MCP-1), and nitric oxide synthase2 (NOS2), and M2 macrophage factors, IL-4, arginase1 (Arg1) and CD163 in AD-like skin, which were confirmed by western blot and ELISA analysis. In addition, PFS inhibited LPS-induced macrophage polarization via the inhibition of the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and nuclear translocation of NF-κB p65. These results suggest that PFS exerted an antidermatitis effect against oxazolone by modulating macrophage activation. PFS administration might be useful in the treatment of AD and inflammatory skin diseases.

Sign in / Sign up

Export Citation Format

Share Document