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Neuroimmunology and Neuroinflammation 2018年第9期5卷 2-14页

作者： Cinzia Dello Russo Natalia Cappoli Institute of Pharmacology UniversitàCattolica del S CuoreRome00168Italy Fondazione Policlinico Gemelli IRCCS 00168RomeItaly

Glioma associated microglia/macrophages (GAMs) constitute the largest proportion of glioma infiltrating cells, par-ticularly in high grade tumors (i.e., glioblastoma). Once inside the tumors, GAMs usually acquire a specific pheno-type of activation that favors tumor growth, angiogenesis and promotes the invasion of normal brain parenchyma. Therefore, treatments that limit or prevent GAMs' recruitment at the tumor site or modulate their immune activa-tion promoting antitumor activities are expected to exert beneficial effects in glioblastoma. In the present paper, we aim at the revision of pharmacological strategies that interfere with GAMs' function and are currently proposed as an alternative/additional option to current approved cytotoxic regimens.

关键词： Glioblastoma macrophages microglia metalloproteases pro-inflammatory activation pro-tumor func-tions glioma associated microglia/macrophages targeted therapies pharmacotherapy

Mitochondrial transfer from MSCs to macrophages restricts inflammation and alleviates kidney injury in diabetic nephropathy mice via PGC-1α activation

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Mitochondrial transfer from MSCs to macrophages restricts in...

第十四届全国免疫学学术大会

作者： Yujia Yuan Jingchao Yang Longhui Yuan Jingqiu Cheng Yanrong Lu Key Laboratory of Transplant Engineering and Immunology West China Hospital Sichuan University West China Hospital Sichuan University

Mesenchymal stem cells(MSCs) have fueled ample translation for treatment of immune-mediated diseases. Our previous study had demonstrated that MSCs could elicit macrophages(Mφ) into anti-inflammatory phenotypes, and alleviate kidney injury in diabetic nephropathy mice via improving mitochondrial function of Mφ, yet the specific mechanism was unclear. Recent evidence indicated that MSCs communicated with their microenvironment through exchanges of mitochondria. By a co-culture system consisting of MSCs and Mφ, we showed that MSCs-derived mitochondria(MSCs-Mito) were transferred into Mφ, and the mitochondrial functions were improved, which contributed to M2 polarization. Furthermore, we found that MSCs-Mito transfer activated peroxisome proliferator-activated receptor gamma coactivator-1 alpha(PGC-1α)-mediated mitochondrial biogenesis. In addition, PGC-1α interacted with TFEB in high glucose(HG)-induced Mφ, leading to the elevated lysosome-autophagy, which was essential to removal of damaged mitochondria. As a result, in Mφ the mitochondrial bioenergy and capacity to combat inflammatory response were enhanced. Whereas, the immune-regulatory activity of MSCs-Mito was significantly blocked in PGC-1α knockdown Mφ. More importantly, MSCs-Mito transfer could be observed in DN mice, and the adoptive transfer of MSCs-Mito educated Mφ(MφMito) inhibited the inflammatory response and alleviated kidney injury. While the kidney-protective effects of MφMito were abolished when the MSCs-Mito was impaired with rotenone(Rot), and the similar Results were also observed when MφMito were transfected with sipgc-1α before administration. Collectively, these findings suggested that MSCs elicited Mφ into anti-inflammatory phenotype and ameliorated kidney injury through mitochondrial transfer in DN mice, and the effects were relied on PGC-1α-mediated mitochondrial biogenesis and PGC-1α/TFEB-mediated lysosome-autophagy.

关键词： mesenchymal stem cells mitochondrial transfer macrophages PGC-1α TFEB

Role of macrophages and monocytes in hepatitis C virus infections

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World Journal of Gastroenterology 2014年第11期20卷 2777-2784页

作者： Dennis Revie Syed Zaki Salahuddin Department of Biology California Lutheran UniversityThousand OaksCA 91360United States California Institute of Molecular Medicine VenturaCA 93003United States

A number of studies conducted over many years have shown that hepatitis C virus(HCV)can infect a variety of cell types.In vivo infection of monocytes,macrophages,and dendritic cells by HCV has been frequently shown by a number of researchers.These studies have demonstrated replication of HCV by detecting the presence of both negative genomic strands and a variety of non-structural HCV proteins in infected cells.In addition,analyses of genome sequences have also shown that different cell types can harbor different HCV variants.Investigators have also done preliminary studies of which cellular genes are affected by HCV infection,but there have not yet been a sufficient number of these studies to understand the effects of infection on these cells.Analyses of in vitro HCV replication have shown that monocytes,macrophages and dendritic cells can be infected by HCV from patient sera or plasma.These studies suggest that entry and cellular locations may vary between different cell types.Some studies suggest that macrophages may preferentially allow HCV genotype 1 to replicate,but macrophages do not appear to select particular hypervariable regions.Overall,these studies agree with a model where monocytes and macrophages act as an amplification system,in which these cells are infected and show few cytopathic effects,but continuously produce HCV.This allows them to produce virus over an extended time and allows its spread to other cell types.

关键词： Hepatitis C virus macrophages Monocytes Dendritic

Piezo1 mediated mechanosensation in bone marrow macrophages promotes vascular niche regeneration after irradiation injury

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Piezo1 mediated mechanosensation in bone marrow macrophages ...

第十四届全国免疫学学术大会

作者： Xiaomei Zhang Lijia Hou Fengjie Li Weiwei Zhang Chun Wu Lixin Xiang Jiuxuan Li Luping Zhou Xiaojie Wang Yang Xiang Yanni Xiao Li Chen Qian Ran Zhongjun Li The Second Affiliated Hospital Army Military Medical University

Background: Hematopoietic stem cells(HSCs) are regulated by the specific hematopoietic microenvironment(niche), composed of various bone marrow cell types. Irradiation and chemotherapy disrupt the HSCs niche, especial vascular niche, causing delayed hematopoietic reconstruction. The resident bone marrow macrophages(Mφ) are essential for HSCs niche to maintain HSCs pool and support HSCs engraftment, but our understanding of the underlying mechanisms remains insufficient. The recovery of sinusoidal vessels is key to vascular niche regeneration and prerequisite for hematopoietic reconstruction. Here, we examined the role of bone marrow Mφ on the recovery of sinusoidal vessels after irradiation injury.Methods: We examined the survival and activation of bone marrow Mφ in C57BL/6 mice after total body irradiation. The resident bone marrow Mφ were depleted by injecting of clodronate-loaded liposome and the hematopoietic reconstruction and sinusoidal regeneration were assessed after irradiation injury using immunofluorescence and flow cytometry. Then ELISA and flow cytometry were used to analyzed the contribution of residual Mφ to bone marrow VEGF-A. Further, transcriptome sequencing, flow cytometry, agonist and inhibitor etc. were conducted to explore the molecular mechanism of Piezo1 mediated mechanical response to upregulate VEGF-A.Results: The resident bone marrow Mφ persist and were M2-like activated after irradiation. Depletion of bone marrow Mφ delayed the recovery of sinusoidal endothelial cells and hematopoietic stem/progenitor cells, aggravated the radiosensitivity of mice. The residual bone marrow Mφ, especial M2-like Mφ, upregulated VEGF-A, which is essential for sinusoidal regeneration after irradiation. Mechanistically, the residual bone marrow Mφ, especial M2-like Mφ, upregulated mechanosensory ion channels Piezo1 and responded to mechanical environment changes induced by bone marrow ablation. Irradiation effect, activation of Piezo1 itself and M2-like polarization induced by phagocytosis of apoptotic cell

关键词： irradiation Piezo1 macrophages sinusoidal regeneration hematopoietic reconstitution

Analysis of the effect of Chlamydia pneumoniae on the lipid metabolism of mononuclear macrophages in patients with carotid atherosclerotic plaque

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Journal of Hainan Medical University 2017年第6期23卷 30-33页

作者： Qing-Di Zeng Ai-Cui Lin Laboratory Department the First People's Hospital of Jining CityJining CityShandong272100 Department of Rehabilitation Medicine the First Hospital Affiliated to Nanjing Medical UniversityNanjingJiangsu210000

Objective:To explore the effect of Chlamydia pneumoniae on the lipid metabolism of mononuclear macrophages in patients with carotid atherosclerotic plaque.Methods: A total of 90 patients with carotid atherosclerosis who were admitted in our hospital from January, 2012 to December, 2013 were included in the study and served as the observation group, while 72 aged individuals at the same stage for physical examination were served as the control group. The plaque formation in the two groups was observed and compared. The levels of TC, LDL-C, and HDL-C in the two groups were detected and compared. ELISA was used to detect CP IgG. The positive rate of CP IgG in the two groups was compared.Results: The multiple plaque, soft plaque, and mixed plaque in the observation group were significantly greater than those in the control group, but the comparison of hard plaque between the two groups was not statistically significant. The levels of TC and LDL-C in the observation group were significantly higher than those in the control group, while HDL-C level was significantly lower than that in the control group. The positive rate of CP IgG in the observation group was significantly higher than that in the control group.Conclusions: Chlamydia pneumoniae has an important effect on the lipid metabolism of mononuclear macrophages in patients with carotid atherosclerotic plaque.

关键词： Chlamydia pneumoniae Carotid atherosclerosis Mononuclear macrophages

Fusion Between Breast Cancer Cells and macrophages Promotes Proliferation and Metastasis of Breast Cancer Cells via PI3K/AKT and MAPK/ERK signaling pathways

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Fusion Between Breast Cancer Cells and Macrophages Promotes ...

中国生物化学与分子生物学会2020全国学术在线会议

作者： Li-Na Zhang Di-Di Zhang Lei Zhao Yu-Xuan Gu Xiao-Lin Sun College of Life Science and Chemistry Faculty of Environment and LifeBeijing University of Technology

Cell fusion is one of the common phenomena in the tumor progression.Studies have shown that tumor cells can fuse with various types of normal cells and participate in the tumorigenesis and metastasis.Cell fusion theory is also considered as a novel mechanism of tumor metastasis.In order to reveal the molecular mechanisms between cell fusion and tumor metastasis,we had successfully conducted a fusion model between breast cancer cells and macrophages.Previous studies found that the fusion hybrids exhibited significantly enhanced proliferation and metastasis abilities.Therefore,we next focus on the effects of cell fusion between breast cancer cells and macrophages on the PI3 K/AKT and MAPK/ERK signaling pathways that are closely related to tumor cell proliferation and metastasis.Western blot results showed that the expression of the key marker proteins of PI3 K/AKT and MAPK/ERK signaling pathways including p-PI3 K,p-AKT and p-ERK1/2 was significantly upregulated in the fused cells.After PI3 K/AKT and MAPK/ERK signaling pathways being blocked by LY294002 and PD98059 inhibitors,the expression of p-AKT and p-ERK1/2 in the fused cells was significantly reduced,and the proliferation,migration and invasion abilities of the fused cells were inhibited.These results suggest that cell fusion between breast cancer cells and macrophages may promote the proliferation and metastasis of breast cancer by activating PI3 K/AKT and MAPK/ERK signaling pathways.Our data also provides new ideas for further understanding the mechanisms of cell fusion in tumorigenesis and metastasis.

关键词： Cell fusion Breast cancer macrophages PI3K/AKT MAPK/ERK

Pristane-induced autophagy activates STAT1/TLR3 pathway in macrophages contributing to experimental arthritis in a Ncf1 dependent manner

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Pristane-induced autophagy activates STAT1/TLR3 pathway in m...

中国生物化学与分子生物学会2020全国学术在线会议

作者： Jing Zhang Wenhua Zhu Liesu Meng Rikard Holmdahl Shemin Lu Institute of Molecular and Translational Medicine Xi'an Jiaotong University Health Science Center Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University) Ministry of Education

We have previously found that pristane could induce autophagy in macrophages,which was associated with STAT1 activation and arthritis development.However,the mechanism whereby pristane regulates autophagy induction and subsequent STAT1 activation remains unclear.In this study,we found that pristane induced ER stress,promoting mTOR degradation,leading to the enhancement of autophagy in macrophages.Both arthritogenic oil adjuvants like pristane and hexadecane,and nonarthritogenic oils like phytol and dodecane,could induce autophagy in macrophages.However,only the former ones,inducing a weak oxidative burst,activated STAT1 and upregulated TLR3 expression,while the latter ones,triggering a strong oxidative burst,failed to activate STAT1/TLR3 pathway.In addition,with pristane injection,macrophages in arthritis-susceptible DA rats(with a Ncf1 allele that allows only low oxidative burst) showed an activated STAT1 pathway,but macrophages in arthritis-resistant DA.Ncf1 congenic rats(with an Ncf1 allele that allows a stronger oxidative burst) showed inactivation in STAT1 pathway.Together,we conclude that pristane,regulating ER stress and mTOR and inducing autophagy,activates STAT1/TLR3 pathway in macrophages and participates in development of arthritis controlled by Ncf1-dependent oxidative burst.

关键词： Experimental arthritis macrophages Ncf1 STAT1 pathway Autophagy

Improving treatment effects of microwave ablation for hepatocellular carcinoma via iron oxide nanoparticles targeting tumor associated macrophages

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Improving treatment effects of microwave ablation for hepato...

中国超声医学工程学会第五届全国介入超声医学学术交流大会

作者：崔瑞中国人民解放军总医院

Objectives:1.To explore the situation of local tumor progression and infiltration of macrophages in peri-ablation zone of mouse model after insufficient microwave ablation.2.To prepare iron oxide nanoparticles Man-IONPs and explore its physicochemical properties,bio-safety,effectiveness in targeting M2 macrophages and inducing pro-inflammatory macrophage polarization.3.To evaluate the inhibitory effect of Man-IONPs on local tumor progression after insufficient microwave ablation.Methods:1.Established an orthotopic liver cancer mouse model,conducted insufficient microwave ablation and observed the local tumor progression after ablation.Explored the infiltration of macrophages and the proportion of M2 macrophages in the peri-ablation zone via immunohistochemistry and immunofluorescence.2.Synthesized Man-IONPS and evaluated its physicochemical properties.The cytotoxicity of Man-IONPs was tested in Hepa 1-6 and RAW264.7 cells,and its biotoxicity was tested in C57 BL6 mice.3.Evaluated the targeting effect of Man-IONPs on M2 macrophages and the peri-ablation zone in mouse model via Prussian blue staining.Verified the efficacy of Man-IONPs in inducing pro-inflammatory macrophage polarization via PCR and ELISA.4.The orthotopic liver cancer model mice were divided into 6 groups-MWA+Man-IONPs group,MWA+IONPs group,MWA group,Control group,Man-IONPs group and IONPs group) to receive corresponding treatment.The changes of tumor volume after ablation were monitored in MR imaging for small animal,and the infiltration of macrophages in the peri-ablation areas were further explored by immunohistochemistry and immunofluorescence staining.Results:1.At 2 weeks after the ablation treatment,local tumor progression occurred around the ablation zone of the mouse model.The number of macrophages in the peri-ablation zone and the proportion of M2 macrophages was significantly increased at 2 weeks after ablation compared with that at 3 days and 1 week after ablation.2.Man-IONPs have good dispersibility and uniform morphology,and the average

关键词： microwave ablation hepatocellular carcinoma iron oxide nanoparticles macrophages

Preliminary analysis of cellular sociology of co-cultured glioma initiating cells and macrophages in vitro

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Translational Neuroscience and Clinics 2016年第2期2卷 77-86页

作者： Mingxia Zhang Junjie Chen Lin Wang Xiaoyan Ji Lin Yang Yujing Sheng Hairui Liu Haiyang Wang Aidong Wang Xingliang Dai Xiaonan Li Qiang Huang Jun Dong Department of Neurology the Second Affiliated Hospital of Soochow University Department of Neurology Xishan People’s Hospital Laboratory of Molecular Neuron-oncology Texas Children’s Cancer Center Baylor College of Medicine

Objective: Real-time monitoring of cytokine secretion at the single immunocyte level,based on the concept of immune cells, sociology has been recently reported. However,the relationships between glioma-initiating cells(GICs) and host immune cells and their mutual interactions in the tumor microenvironment have not been directly observed and remain unclear. Methods: The dual fluorescence tracing technique was applied to label the co-cultured GICs and host macrophages(M?), and the interactions between the two types of cells were observed using a live cell imaging system. Fusion cells in the co-culture system were monocloned and proliferated in vitro and their social interactions were observed and recorded. Results: Using real-time dynamic observation of target cells, 6 types of intercellular conjunction microtubes were found to function in the transfer of intercellular information between GICs and M?; GICs and host M? can fuse into hybrid cells after several rounds of mutual interactions, and then these fusion cells fused with each other; Fusion cells generated offspring cells through symmetrical and asymmetrical division or underwent apoptosis. A "cell in cell" phenomenon was observed in the fusion cells, which was often followed by cell release, namely entosis. Conclusions: Preliminary studies revealed the patterns of cell conjunction via microtubes between GICs and host M? and the processes of cell fusion, division, and entosis. The results revealed malignant transformation of host M?, induced by GICs, suggesting complex social relationships among tumor-immune cells in gliomas.

关键词： glioma initiating cells macrophages cellular interactions live cell time-lapse shoot dual fluorescence tracing technique

To investigate the role of macrophages in the development of murine pulmonary fibrosis induced irradiation exposure

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To investigate the role of macrophages in the development of...

第十四届中国实验动物科学年会

作者： Lulu Su Deguan li Yinping Dong Yueying Wang Yuquan Wang Bowen Guan Yanhua Lu Feiyue Fan Aimin Meng Institute of Laboratory Animal Science Chinese Academy of Medical Science (CAMS) and Comparative Medicine Center Peking Union Medical College (PUMC) Key Laboratory of Human Diseases Comparative Medicine Ministry of Health Beijing Key Laboratory for Animal Models of Emerging and Remerging Infectious Diseases Beijing Engineering Research Center for Laboratory Animal Models of Human Critical Diseases Institute of Radiation Medicine Chinese Academy of Medical Science and Peking Union Medical College Tianjin Key Laboratory of Radiation Medicine and Molecular Nuclear Medicine

Purpose:Radiation induced pulmonary fibrosis(RIPF) is one of the severe injuries induced by irradiation exposure. The pathogenesis of RIPF is very complicated. The present study was to investigate the changes of phenotype of macrophages and genes expression, and explore the effect of irradiation on the function of macrophages in the development of RIPF. Methods: The C57 BL/6 male mice were exposed to 17 Gy X ray irradiation(IR) on the right side of the chest to establish lung fibrosis model. ABT-263 was a BCL-2 inhibitor and found to attenuate RIPF in our previous work. ABT-263 was administered at 16 weeks post IR exposure. The right lung tissues were collected at 4, 8, 16 and 23 weeks post IR to detect the alternation of phenotype of macrophages by flow cytometry. RT-PCR was used to detect genes expression level of sorted macrophages in the right lung at various time-points. Results:(1) During the development of RIPF, the ratio of macrophages in the right lung tissue had no changes between control group and IR group.(2) Compared with the control group, the MFI of M2 macrophages of IR group was significantly decreased at 8 weeks, and increased at 16 weeks and 23 weeks post IR. However, there were no significant differences in the MFI of M1 macrophages between control group and IR group at various time-points.(3) The expression level of P16 in sorted macrophages from irradiated mice significantly increased but the expression level of P21 didn’t change during lung fibrosis. As to the genes related to the function of M1 and M2 macrophage, the expression levels of TGF-α,IL-1α,IL-10, Arg-1 and Mmp14 significantly increased, especially in the late stage of fibrosis development. However, the expression level of TGF-β had no change during fibrosis, which was the most common pro-fibrotic factor.(4) ABT-263 had no function on the ratio of macrophage, macrophage polarization and genes expression at 23 weeks post IR. Discussion:In this study, we found macrophage polarization was changed after pulmonary irradiation exposure.

关键词： Radiation induced pulmonary fibrosis Irradiation macrophages ABT-263