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首页> 外文期刊>Infection and immunity >Toll-Like Receptor Prestimulation Increases Phagocytosis of Escherichia coli DH5α and Escherichia coli K1 Strains by Murine Microglial Cells
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Toll-Like Receptor Prestimulation Increases Phagocytosis of Escherichia coli DH5α and Escherichia coli K1 Strains by Murine Microglial Cells

机译：Toll样受体预刺激增加鼠小胶质细胞吞噬大肠杆菌DH5α和大肠杆菌K1菌株的吞噬作用。

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Meningitis and meningoencephalitis caused by Escherichia coli are associated with high rates of mortality. When an infection occurs, Toll-like receptors (TLRs) expressed by microglial cells can recognize pathogen-associated molecular patterns and activate multiple steps in the inflammatory response that coordinate the brain's local defense, such as phagocytosis of invading pathogens. An upregulation of the phagocytic ability of reactive microglia could improve the host defense in immunocompromised patients against pathogens such as E. coli. Here, murine microglial cultures were stimulated with the TLR agonists Pam3CSK4 (TLR1/TLR2), lipopolysaccharide (TLR4), and CpG oligodeoxynucleotide (TLR9) for 24 h. Upon stimulation, levels of tumor necrosis factor alpha and the neutrophil chemoattractant CXCL1 were increased, indicating microglial activation. Phagocytic activity was studied after adding either E. coli DH5α or E. coli K1 strains. After 60 and 90 min of bacterial exposure, the number of ingested bacteria was significantly higher in cells prestimulated with TLR agonists than in unstimulated controls (P < 0.01). Addition of cytochalasin D, an inhibitor of actin polymerization, blocked >90% of phagocytosis. We also analyzed the ability of microglia to kill the ingested E. coli strains. Intracellularly surviving bacteria were quantified at different time points (90, 150, 240, and 360 min) after 90 min of phagocytosis. The number of bacteria killed intracellularly after 6 h was higher in cells primed with the different TLR agonists than in unstimulated microglia. Our data suggest that microglial stimulation by the TLR system can increase bacterial phagocytosis and killing. This approach could improve central nervous system resistance to infections in immunocompromised patients.
机译：大肠杆菌引起的脑膜炎和脑膜脑炎与高死亡率有关。当发生感染时，小胶质细胞表达的Toll样受体（TLR）可以识别病原体相关的分子模式，并激活炎症反应的多个步骤，从而协调大脑的局部防御，例如入侵病原体的吞噬作用。反应性小胶质细胞吞噬能力的上调可以改善免疫受损患者抵抗病原体（如Em）的宿主防御能力。大肠杆菌。在这里，用TLR激动剂Pam 3 CSK 4 （TLR1 / TLR2），脂多糖（TLR4）和CpG寡脱氧核苷酸（TLR9）刺激小鼠小胶质细胞培养24小时。刺激后，肿瘤坏死因子α和嗜中性粒细胞趋化因子CXCL1的水平增加，表明小胶质细胞活化。在加入任一 E后研究吞噬活性。大肠菌DH5α或 E。大肠杆菌K1菌株。在细菌暴露60和90分钟后，用TLR激动剂预刺激的细胞中摄入的细菌数量显着高于未刺激的对照组（ P <0.01）。加入细胞松弛素D（肌动蛋白聚合的抑制剂）可阻止> 90％的吞噬作用。我们还分析了小胶质细胞杀死摄入的 E的能力。大肠杆菌菌株。在吞噬作用90分钟后的不同时间点（90、150、240和360分钟）对细胞内存活细菌进行定量。用不同的TLR激动剂引发的细胞在6 h后细胞内杀死的细菌数量要比未刺激的小胶质细胞高。我们的数据表明，TLR系统对小胶质细胞的刺激可以增加细菌的吞噬作用和杀伤力。这种方法可以提高中枢神经系统对免疫功能低下患者感染的抵抗力。

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