Macrophage最新文献

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Macrophage cell death upon intracellular bacterial infection. 细胞内细菌感染导致巨噬细胞死亡。
Macrophage Pub Date : 2015-04-26 DOI: 10.14800/MACROPHAGE.779
Xin-He Lai, Yunsheng Xu, Xiao-ming Chen, Yi Ren
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引用次数: 12
New macrophage models of Gaucher disease offer new tools for drug development. 新的戈谢病巨噬细胞模型为药物开发提供了新的工具。
Macrophage Pub Date : 2015-04-07 DOI: 10.14800/MACROPHAGE.712
Daniel K. Borger, E. Sidransky, E. Aflaki
{"title":"New macrophage models of Gaucher disease offer new tools for drug development.","authors":"Daniel K. Borger, E. Sidransky, E. Aflaki","doi":"10.14800/MACROPHAGE.712","DOIUrl":"https://doi.org/10.14800/MACROPHAGE.712","url":null,"abstract":"Gaucher disease is an inherited enzyme deficiency resulting in the lysosomal accumulation of specific glycolipids in macrophages and, in some cases, neurons. While current treatments are effective at reducing this glycolipid storage in macrophages, they are expensive and ineffective in treating neurological manifestations of the disease, driving the search for novel therapeutics. Moreover, mutations in GBA1, the gene implicated in Gaucher disease, are an important risk factor for the development of Parkinson disease and related disorders, an association that has further heightened interest in Gaucher disease research. However, the development of therapeutic strategies has been hampered by a shortage of appropriate cellular models of Gaucher disease. We have generated two novel macrophage models of Gaucher disease, one through the differentiation of peripheral blood monocytes from patients with Gaucher disease and the other through the differentiation of induced pluripotent stem cells derived from patient fibroblasts. Both disease models demonstrate similar cellular phenotypes and exhibit extensive glycolipid storage when exposed to exogenous lipid sources such as erythrocyte membranes. Furthermore, we have used these models to confirm the efficacy of a novel small molecule in clearing glycolipid storage and restoring normal macrophage function. These results demonstrate the usefulness of these models in exploring new therapeutics for Gaucher disease and related disorders.","PeriodicalId":90918,"journal":{"name":"Macrophage","volume":"2 1 1","pages":"e712"},"PeriodicalIF":0.0,"publicationDate":"2015-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66657183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 5
Macrophage polarization in kidney diseases. 肾脏疾病中的巨噬细胞极化。
Macrophage Pub Date : 2015-01-01 DOI: 10.14800/macrophage.679
Shaojiang Tian, Shi-You Chen
{"title":"Macrophage polarization in kidney diseases.","authors":"Shaojiang Tian,&nbsp;Shi-You Chen","doi":"10.14800/macrophage.679","DOIUrl":"https://doi.org/10.14800/macrophage.679","url":null,"abstract":"<p><p>Macrophage accumulation associates closely with the degree of renal structural injury and renal dysfunction in human kidney diseases. Depletion of macrophages reduces while adoptive transfer of macrophages worsens inflammation in animal models of the renal injury. However, emerging evidence support that macrophage polarization plays a critical role in the progression of a number of kidney diseases including obstructive nephropathy, ischemia-reperfusion injury, glomerulonephritis, diabetic nephropathy, and other kidney diseases. In this mini-review, we briefly summarize the macrophage infiltration and polarization in these inflammatory and fibrotic kidney diseases, discussing the results mostly from studies in animal models. In view of the critical role of macrophage in the progression of these diseases, manipulating macrophage phenotype may be a potential effective strategy to treat various kidney diseases.</p>","PeriodicalId":90918,"journal":{"name":"Macrophage","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.14800/macrophage.679","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33275599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 42
New macrophage models of Gaucher disease offer new tools for drug development. 新的戈谢病巨噬细胞模型为药物开发提供了新的工具。
Macrophage Pub Date : 2015-01-01
Daniel K Borger, Ellen Sidransky, Elma Aflaki
{"title":"New macrophage models of Gaucher disease offer new tools for drug development.","authors":"Daniel K Borger,&nbsp;Ellen Sidransky,&nbsp;Elma Aflaki","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Gaucher disease is an inherited enzyme deficiency resulting in the lysosomal accumulation of specific glycolipids in macrophages and, in some cases, neurons. While current treatments are effective at reducing this glycolipid storage in macrophages, they are expensive and ineffective in treating neurological manifestations of the disease, driving the search for novel therapeutics. Moreover, mutations in <i>GBA1</i>, the gene implicated in Gaucher disease, are an important risk factor for the development of Parkinson disease and related disorders, an association that has further heightened interest in Gaucher disease research. However, the development of therapeutic strategies has been hampered by a shortage of appropriate cellular models of Gaucher disease. We have generated two novel macrophage models of Gaucher disease, one through the differentiation of peripheral blood monocytes from patients with Gaucher disease and the other through the differentiation of induced pluripotent stem cells derived from patient fibroblasts. Both disease models demonstrate similar cellular phenotypes and exhibit extensive glycolipid storage when exposed to exogenous lipid sources such as erythrocyte membranes. Furthermore, we have used these models to confirm the efficacy of a novel small molecule in clearing glycolipid storage and restoring normal macrophage function. These results demonstrate the usefulness of these models in exploring new therapeutics for Gaucher disease and related disorders.</p>","PeriodicalId":90918,"journal":{"name":"Macrophage","volume":"2 1","pages":"e712"},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4469193/pdf/nihms689401.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33400604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Post-infectious inflammatory response syndrome (PIIRS): Dissociation of T-cell-macrophage signaling in previously healthy individuals with cryptococcal fungal meningoencephalitis. 感染后炎症反应综合征(PIIRS):先前健康的隐球菌真菌脑膜脑炎患者中t细胞-巨噬细胞信号的分离
Macrophage Pub Date : 2015-01-01 Epub Date: 2015-11-23 DOI: 10.14800/Macrophage.1078
Peter R Williamson
{"title":"Post-infectious inflammatory response syndrome (PIIRS): Dissociation of T-cell-macrophage signaling in previously healthy individuals with cryptococcal fungal meningoencephalitis.","authors":"Peter R Williamson","doi":"10.14800/Macrophage.1078","DOIUrl":"https://doi.org/10.14800/Macrophage.1078","url":null,"abstract":"<p><p><i>Cryptococcus</i> is an important cause of central nervous system infections in both immunocompromised patients such as those with HIV/AIDS as well as previously healthy individuals. Deficiencies in T-cell activation are well-known to be highly associated with host susceptibility in HIV/AIDS as well in animal modeling studies, resulting in poor microbiological control and little host inflammation. However, recent studies conducted in human patients have demonstrated roles for macrophage signaling defects as an important association with disease susceptibility. For example, an autoantibody to granulocyte monocyte stimulating factor (GMCSF) resulted in defective STAT5 signaling and susceptibility to cryptococcosis. In addition, severe cases of cryptococcal meningo-encephalitis in previously healthy patients, with or without anti-GMCSF autoantibody, developed a highly activated intrathecal T-cell population but had defects in effective macrophage polarization. Intrathecal inflammation correlated with neurological damage, measured by the axonal damage protein, neurofilament light chain 1. Based on these studies, we propose a new syndrome of cryptococcal post-infectious inflammatory response syndrome (PIIRS) defined in previously healthy patients with cryptococcal meningo-encephalitis as the presence of a poor clinical response in the setting of at least 1 month of amphotericin-based fungicidal therapy and sterile cerebrospinal cultures. These findings are discussed in light of the potential for improving therapy.</p>","PeriodicalId":90918,"journal":{"name":"Macrophage","volume":"2 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.14800/Macrophage.1078","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34740335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 20
Interleukin-19 can enhance angiogenesis by Macrophage Polarization. 白细胞介素-19可通过巨噬细胞极化促进血管生成。
Macrophage Pub Date : 2015-01-01 DOI: 10.14800/macrophage.562
Khatuna Gabunia, Michael V Autieri
{"title":"Interleukin-19 can enhance angiogenesis by Macrophage Polarization.","authors":"Khatuna Gabunia,&nbsp;Michael V Autieri","doi":"10.14800/macrophage.562","DOIUrl":"https://doi.org/10.14800/macrophage.562","url":null,"abstract":"<p><p>Hypoxia in ischemic limbs typically initiates angiogenic and inflammatory factors to promote angiogenesis in attempt to restore perfusion, and revascularization involves multiple cell types and systems. Macrophage display phenotype plasticity, and can polarize in response to local and systemic cytokine stimuli. M2 macrophage are known to play an important role in angiogenesis and wound healing. While accepted that many pro-inflammatory cytokines induce angiogenesis, the effects of anti-inflammatory interleukins on initiation of angiogenesis are less clear. Interleukin-19 [IL-19] is a presumed anti-inflammatory cytokine, with unknown effects on macrophage polarization. In our recent study, we used several experimental approaches and determined that IL-19 regulated neovascularization in the murine hind-limb ischemia model. In addition to endothelial cells, we found that IL-19 could target and polarize macrophage to the M2 phenotype. IL-19 could induce expression of angiogenic, and reduce expression of anti-angiogenic cytokines in these cells. This is the first study to demonstrate that IL-19 could polarize macrophage, and potentially identifies IL-19 as a therapy to induce angiogenesis in ischemic tissue.</p>","PeriodicalId":90918,"journal":{"name":"Macrophage","volume":"2 1","pages":"e562"},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.14800/macrophage.562","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33350153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Retinal phagocytes in age-related macular degeneration. 视网膜吞噬细胞在年龄相关性黄斑变性中的作用。
Macrophage Pub Date : 2015-01-01 DOI: 10.14800/macrophage.698
Soo-Young Kim
{"title":"Retinal phagocytes in age-related macular degeneration.","authors":"Soo-Young Kim","doi":"10.14800/macrophage.698","DOIUrl":"https://doi.org/10.14800/macrophage.698","url":null,"abstract":"<p><p>Age-related macular degeneration (AMD) is the leading cause of blindness in industrial countries. Vision loss caused by AMD results from geographic atrophy (dry AMD) and/or choroidal neovascularization (wet AMD). Presently, the etiology and pathogenesis of AMD is not fully understood and there is no effective treatment. Oxidative stress in retinal pigment epithelial (RPE) cells is considered to be one of the major factors contributing to the pathogenesis of AMD. Also retinal glia, as scavengers, are deeply related with diseases and could play a role. Therefore, therapeutic approaches for microglia and Müller glia, as well as RPE, may lead to new strategies for AMD treatment. This review summarizes the pathological findings observed in RPE cells, microglia and Müller glia of AMD murine models.</p>","PeriodicalId":90918,"journal":{"name":"Macrophage","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4457466/pdf/nihms689403.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33248928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 17
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