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首页> 外文期刊>Infection and immunity >In Vitro Characterization of the Microglial Inflammatory Response to Streptococcus suis, an Important Emerging Zoonotic Agent of Meningitis
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In Vitro Characterization of the Microglial Inflammatory Response to Streptococcus suis, an Important Emerging Zoonotic Agent of Meningitis

机译：猪链球菌，脑膜炎的一种重要的人畜共患病原体的小胶质细胞炎症反应的体外表征。

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Streptococcus suis is an important swine and human pathogen responsible for septicemia and meningitis. In vivo research in mice suggested that in the brain, microglia might be involved in activating the inflammatory response against S. suis. The aim of this study was to better understand the interactions between S. suis and microglia. Murine microglial cells were infected with a virulent wild-type strain of S. suis. Two isogenic mutants deficient at either capsular polysaccharide (CPS) or hemolysin production were also included. CPS contributed to S. suis resistance to phagocytosis and regulated the inflammatory response by hiding proinflammatory components from the bacterial cell wall, while the absence of hemolysin, a potential cytotoxic factor, did not have a major impact on S. suis interactions with microglia. Wild-type S. suis induced enhanced expression of Toll-like receptor 2 by microglial cells, as well as phophotyrosine, protein kinase C, and different mitogen-activated protein kinase signaling events. However, cells infected with the CPS-deficient mutant showed overall stronger and more sustained phosphorylation profiles. CPS also modulated inducible nitric oxide synthase expression and further nitric oxide production from S. suis-infected microglia. Finally, S. suis-induced NF-κB translocation was faster for cells stimulated with the CPS-deficient mutant, suggesting that bacterial cell wall components are potent inducers of NF-κB. These results contribute to increase the knowledge of mechanisms underlying S. suis inflammation in the brain and will be useful in designing more efficient anti-inflammatory strategies for meningitis.
机译：猪链球菌是引起败血病和脑膜炎的重要猪和人类病原体。小鼠体内研究表明，在大脑中，小胶质细胞可能参与了针对猪链球菌的炎症反应。这项研究的目的是更好地了解猪链球菌和小胶质细胞之间的相互作用。鼠小胶质细胞被有毒的猪链球菌野生型菌株感染。还包括两个荚膜多糖（CPS）或溶血素产生缺陷的同基因突变体。 CPS有助于猪链球菌对吞噬作用的抗性并通过​​从细菌细胞壁中隐藏促炎成分来调节炎症反应，而缺少溶血素（一种潜在的细胞毒性因子）对猪链球菌与小胶质细胞的相互作用没有重大影响。野生型猪链球菌诱导小胶质细胞以及磷酪氨酸，蛋白激酶C和不同的促分裂原活化蛋白激酶信号转导事件增强了Toll样受体2的表达。但是，感染了CPS缺陷突变体的细胞显示出总体上更强和更持久的磷酸化谱。 CPS还调节了诱导型一氧化氮合酶的表达，并进一步控制了由猪链球菌感染的小胶质细胞产生的一氧化氮。最后，对于CPS缺陷型突变体刺激的细胞，猪链球菌诱导的NF-κB转运更快，表明细菌细胞壁成分是NF-κB的有效诱导剂。这些结果有助于增加人们对猪链球菌炎症机制的认识，并将有助于设计针对脑膜炎的更有效的抗炎策略。

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