Targeted ferritin nanoparticle encapsulating CpG oligodeoxynucleotides induces tumor-associated macrophage M2 phenotype polarization into M1 phenotype and inhibits tumor growth

Nanoscale ◽  
2020 ◽  
Vol 12 (43) ◽  
pp. 22268-22280
Author(s):  
Hui Shan ◽  
Wenlong Dou ◽  
Yu Zhang ◽  
Mi Qi
Keyword(s):  
Tumor Growth ◽  
Intravenous Injection ◽  
Inhibit Tumor Growth ◽  
Cpg Oligodeoxynucleotides ◽  
Tumor Associated Macrophage ◽  
M1 Phenotype ◽  
M1 Type ◽  
M2 Phenotype

Novel M2pep-rHF-CpG nanoparticles repolarize the M2-type TAMs to M1-type and inhibit tumor growth after intravenous injection.

Polarization of tumor-associated macrophage phenotype via porous hollow iron nanoparticles for tumor immunotherapy in vivo

Nanoscale ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 130-144 ◽  
Author(s):  
Ke Li ◽  
Lu Lu ◽  
Chencheng Xue ◽  
Ju Liu ◽  
Ye He ◽  
...  
Keyword(s):  
Immune Response ◽  
Tumor Growth ◽  
Iron Nanoparticles ◽  
Tumor Immunotherapy ◽  
Macrophage Phenotype ◽  
Tumor Associated Macrophage ◽  
Immunosuppressive Microenvironment ◽  
M1 Type

PHNPs and 3-MA re-polarize TAMs to M1-type by activating the protein of NF-κB p65 and then remodelling the immunosuppressive microenvironment, thus activating immune response and inhibiting tumor growth.

scholarly journals Pinosylvin Shifts Macrophage Polarization to Support Resolution of Inflammation

Molecules ◽  
2021 ◽  
Vol 26 (9) ◽  
pp. 2772
Author(s):  
Konsta Kivimäki ◽  
Tiina Leppänen ◽  
Mari Hämäläinen ◽  
Katriina Vuolteenaho ◽  
Eeva Moilanen
Keyword(s):  
Macrophage Activation ◽  
Environmental Changes ◽  
Macrophage Polarization ◽  
Resolution Of Inflammation ◽  
Human Macrophages ◽  
Arginase 1 ◽  
M1 Phenotype ◽  
Anti Inflammatory ◽  
M1 Type ◽  
M2 Phenotype

Pinosylvin is a natural stilbenoid found particularly in Scots pine. Stilbenoids are a group of phenolic compounds identified as protective agents against pathogens for many plants. Stilbenoids also possess health-promoting properties in humans; for instance, they are anti-inflammatory through their suppressing action on proinflammatory M1-type macrophage activation. Macrophages respond to environmental changes by polarizing towards proinflammatory M1 phenotype in infection and inflammatory diseases, or towards anti-inflammatory M2 phenotype, mediating resolution of inflammation and repair. In the present study, we investigated the effects of pinosylvin on M2-type macrophage activation, aiming to test the hypothesis that pinosylvin could polarize macrophages from M1 to M2 phenotype to support resolution of inflammation. We used lipopolysaccharide (LPS) to induce M1 phenotype and interleukin-4 (IL-4) to induce M2 phenotype in J774 murine and U937 human macrophages, and we measured expression of M1 and M2-markers. Interestingly, along with inhibiting the expression of M1-type markers, pinosylvin had an enhancing effect on the M2-type activation, shown as an increased expression of arginase-1 (Arg-1) and mannose receptor C type 1 (MRC1) in murine macrophages, and C-C motif chemokine ligands 17 and 26 (CCL17 and CCL26) in human macrophages. In IL-4-treated macrophages, pinosylvin enhanced PPAR-γ expression but had no effect on STAT6 phosphorylation. The results show, for the first time, that pinosylvin shifts macrophage polarization from the pro-inflammatory M1 phenotype towards M2 phenotype, supporting resolution of inflammation and repair.

scholarly journals G1T48, an oral selective estrogen receptor degrader, and the CDK4/6 inhibitor lerociclib inhibit tumor growth in animal models of endocrine-resistant breast cancer

2020 ◽  
Vol 180 (3) ◽  
pp. 635-646 ◽  
Author(s):  
Kaitlyn J. Andreano ◽  
Suzanne E. Wardell ◽  
Jennifer G. Baker ◽  
Taylor K. Desautels ◽  
Robert Baldi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Animal Models ◽  
Tumor Growth ◽  
Inhibit Tumor Growth

scholarly journals Polysaccharides to Inhibit Tumor Growth

1989 ◽  
Vol 7 (12) ◽  
pp. 1222-1222
Author(s):  
Bernard Dixon
Keyword(s):  
Tumor Growth ◽  
Inhibit Tumor Growth

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.

Abstract T P80: Inhibition of Ezh2 Leads to Decreased M1 and Enhanced M2 Microglia Phenotypes

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Edward Koellhoffer ◽  
Jeremy Grenier ◽  
Rodney Ritzel ◽  
Louise McCullough
Keyword(s):  
Ischemic Stroke ◽  
Pcr Analysis ◽  
M2 Polarization ◽  
M2 Microglia ◽  
M1 Polarization ◽  
Glial Cultures ◽  
M2 Response ◽  
M1 Phenotype ◽  
Cayman Chemical ◽  
M2 Phenotype

Background: Ischemic stroke results in the activation of microglia, which may polarize toward a pro-inflammatory (M1) phenotype or an anti-inflammatory, neuroprotective (M2) phenotype. Thus, simultaneously suppressing the M1 response and promoting the M2 response could be beneficial in the treatment of stroke. Recently, the epigenetic modulator Jmjd3 has been shown to be essential for M2 polarization. However, Jmjd3 is antagonized by Ezh2 which is associated with M1 polarization. Thus, we hypothesized that inhibition of Ezh2 tilts the balance between Jmjd3 and Ezh2, thereby enhancing polarization toward an M2 phenotype and improved outcome in ischemic stroke. Methods: Mixed glial cultures were isolated from P0.5-P2 C57BL/6J mice and cultured for 14 days before microglial isolation. Microglia were rested for 24 hours before treatment every other day with 6uM GSK343 (Cayman Chemical) or DMSO vehicle control. After 7 days, microglia were stimulated with LPS or IL-4 and RNA was isolated at 4hr and 24hr post-stimulation for qRT-PCR analysis. Results: LPS-induced IL6 and IL1B expression was significantly abrogated by 71% and 53%, respectively (p<0.05), at 24hr when Ezh2 was inhibited. Additionally, Ezh2 inhibition both increased baseline expression of M2-associated genes ARG1, CD206, and IRF4 by 196%, 257%, and 395%, respectively (p<0.05), and rescued their expression in the presence of LPS at 24hr (p<0.05) in which they were otherwise significantly down-regulated. Conclusion: Pharmacological inhibition of Ezh2 limits microglial M1 polarization and enhances M2 polarization.

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