The ischemic environment drives microglia and macrophage function.
The ischemic environment drives microglia and macrophage function.
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DOI：
10.3389/fneur.2015.00081
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发表时间：
2015
影响因子：
3.4
通讯作者：
De Simoni MG
中科院分区：
文献类型：
--
作者：
Fumagalli S;Perego C;Pischiutta F;Zanier ER;De Simoni MG
髓源性细胞，如小胶质细胞和巨噬细胞，在病理生理过程中在几种炎症机制的交叉点起作用。除了促炎活性（M1极化），髓样细胞获得保护功能（M2），并参与脑损伤后的神经保护先天机制。实验研究正在做出相当大的努力来了解调节有毒和保护性大脑先天免疫之间平衡的规则。环境变化影响小胶质细胞/巨噬细胞功能。缺氧可影响骨髓细胞的分布、活性和表型。小胶质细胞和巨噬细胞因其内在的差异，对缺氧的反应不同，前者依赖ATP激活，后者转换为无氧代谢和适应缺氧。髓样细胞的功能包括稳态控制、损伤感应活性、趋化性和吞噬作用，这些细胞的所有显著特征。特定的标记物和形态能够识别每种功能状态。为了确保体内平衡并在需要时激活，小胶质细胞/巨噬细胞生理学被微调。小胶质细胞由几种神经元衍生的成分控制，包括接触依赖性抑制信号和可溶性分子。这种控制的变化可能导致慢性激活或引发特定的功能后果。策略，如干细胞治疗，可以增强小胶质细胞保护极化。这篇综述介绍了文献中的数据，这些数据极大地促进了我们对髓系细胞在脑损伤中作用的理解。我们讨论了小胶质细胞和巨噬细胞对中风后缺氧的选择性反应，并回顾了相关的标志物，目的是定义被招募到受伤部位的髓样细胞的不同亚群。我们还涵盖了长期活跃的小胶质细胞的功能后果，并回顾了小胶质细胞调节的关键工作，为急性脑损伤提供了新的治疗可能性。
Cells of myeloid origin, such as microglia and macrophages, act at the crossroads of several inflammatory mechanisms during pathophysiology. Besides pro-inflammatory activity (M1 polarization), myeloid cells acquire protective functions (M2) and participate in the neuroprotective innate mechanisms after brain injury. Experimental research is making considerable efforts to understand the rules that regulate the balance between toxic and protective brain innate immunity. Environmental changes affect microglia/macrophage functions. Hypoxia can affect myeloid cell distribution, activity, and phenotype. With their intrinsic differences, microglia and macrophages respond differently to hypoxia, the former depending on ATP to activate and the latter switching to anaerobic metabolism and adapting to hypoxia. Myeloid cell functions include homeostasis control, damage-sensing activity, chemotaxis, and phagocytosis, all distinctive features of these cells. Specific markers and morphologies enable to recognize each functional state. To ensure homeostasis and activate when needed, microglia/macrophage physiology is finely tuned. Microglia are controlled by several neuron-derived components, including contact-dependent inhibitory signals and soluble molecules. Changes in this control can cause chronic activation or priming with specific functional consequences. Strategies, such as stem cell treatment, may enhance microglia protective polarization. This review presents data from the literature that has greatly advanced our understanding of myeloid cell action in brain injury. We discuss the selective responses of microglia and macrophages to hypoxia after stroke and review relevant markers with the aim of defining the different subpopulations of myeloid cells that are recruited to the injured site. We also cover the functional consequences of chronically active microglia and review pivotal works on microglia regulation that offer new therapeutic possibilities for acute brain injury.
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影响因子：
4.2
作者：
Bachstetter, Adam D.;Morganti, Josh M.;Jernberg, Jennifer;Schlunk, Andrea;Mitchell, Staten H.;Brewster, Kaelin W.;Hudson, Charles E.;Cole, Michael J.;Harrison, Jeffrey K.;Bickford, Paula C.;Gemma, Carmelina
通讯作者：
Gemma, Carmelina
影响因子：
16.2
作者：
Bhaskar, Kiran;Konerth, Megan;Kokiko-Cochran, Olga N.;Cardona, Astrid;Ransohoff, Richard M.;Lamb, Bruce T.
通讯作者：
Lamb, Bruce T.
影响因子：
82.9
作者：
Ceradini, DJ;Kulkarni, AR;Gurtner, GC
通讯作者：
Gurtner, GC
影响因子：
4
作者：
Awada, Rana;Saulnier-Blache, Jean Sebastien;Gres, Sandra;Bourdon, Emmanuel;Rondeau, Philippe;Parimisetty, Avinash;Orihuela, Ruben;Harry, G. Jean;d'Hellencourt, Christian Lefebvre
通讯作者：
d'Hellencourt, Christian Lefebvre
影响因子：
5.3
作者：
Blomster, Linda V.;Brennan, Faith H.;Ruitenberg, Marc J.
通讯作者：
Ruitenberg, Marc J.