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首页> 外文期刊>The European Journal of Neuroscience >Interferon-gamma differentially modulates the release of cytokines and chemokines in lipopolysaccharide- and pneumococcal cell wall-stimulated mouse microglia and macrophages.
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Interferon-gamma differentially modulates the release of cytokines and chemokines in lipopolysaccharide- and pneumococcal cell wall-stimulated mouse microglia and macrophages.

机译：干扰素-γ差异性调节脂多糖和肺炎球菌细胞壁刺激的小鼠小胶质细胞和巨噬细胞中细胞因子和趋化因子的释放。

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摘要

During bacterial infections of the CNS, activated microglia could support leucocyte recruitment to the brain through the synthesis of cyto- and chemokines. In turn, invading leucocytes may feedback on microglial cells to influence their chemokine release pattern. Here, we analyzed the capacity of interferon-gamma (IFNgamma) to serve as such a leucocyte-to-microglia signal. Production of cyto- and chemokines was stimulated in mouse microglia cultures by treatments with lipopolysaccharide (LPS) from Gram-negative Escherichia coli or cell walls from Gram-positive Streptococcus pneumoniae (PCW). IFNgamma presence during the stimulation (0.1-100 ng/mL) modulated the patterns of LPS- and PCW-induced cyto- and chemokine release in a dose-dependent, potent and complex manner. While amounts of TNFalpha and IL-6 remained nearly unchanged, IFNgamma enhanced the production of IL-12, MCP-1 and RANTES, but attenuated that of KC, MIP-1alpha and MIP-2. Release modulation was obtained with IFNgamma preincubation (treatment of cells before LPS or PCW administration), coincubation and even delayed addition to an ongoing LPS or PCW stimulation. Together the changes observed for the microglial chemokine release under IFNgamma would shift the chemoattractive profile from favouring neutrophils to a preferential attraction of monocytes and T lymphocyte populations--as actually seen during the course of bacterial meningitis. The findings support the view of activated microglia as a major intrinsic source for an instant production of a variety of chemokines and suggest that leucocyte-derived IFNgamma could potentially regulate the microglial chemokine release pattern.
机译：在中枢神经系统的细菌感染期间，活化的小胶质细胞可以通过细胞因子和趋化因子的合成来支持白细胞向大脑的募集。反过来，入侵的白细胞可能会反馈小胶质细胞以影响其趋化因子释放模式。在这里，我们分析了干扰素-γ（IFNgamma）作为白细胞对小胶质细胞信号的能力。在小鼠小胶质细胞培养物中，通过用革兰氏阴性大肠杆菌的脂多糖（LPS）或肺炎性革兰氏阳性链球菌（PCW）的细胞壁处理，可以刺激细胞和趋化因子的产生。刺激期间IFNγ的存在（0.1-100 ng / mL）以剂量依赖性，有效且复杂的方式调节LPS和PCW诱导的细胞因子和趋化因子释放的模式。尽管TNFalpha和IL-6的量几乎保持不变，但IFNgamma增强了IL-12，MCP-1和RANTES的产生，但减弱了KC，MIP-1alpha和MIP-2的产生。通过IFNγ预培养（在LPS或PCW施用前对细胞进行处理），共培养甚至延迟添加到正在进行的LPS或PCW刺激中来获得释放调节。如在细菌性脑膜炎的过程中实际看到的，在γ干扰素作用下观察到的小胶质细胞趋化因子释放的变化将使趋化特性从偏爱中性粒细胞转移到单核细胞和T淋巴细胞群的优先吸引。这些发现支持了活化的小胶质细胞作为立即产生各种趋化因子的主要内在来源的观点，并表明白细胞衍生的IFNgamma可能调节小胶质细胞趋化因子的释放模式。

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