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Important Role for Toll-Like Receptor 9 in Host Defense against Meningococcal Sepsis

机译：Toll样受体9在宿主抵抗脑膜炎球菌败血症中的重要作用

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Neisseria meningitidis is a leading cause of meningitis and sepsis. The pathogenesis of meningococcal disease is determined by both bacterial virulence factors and the host inflammatory response. Toll-like receptors (TLRs) are prominent activators of the inflammatory response, and TLR2, -4, and -9 have been reported to be involved in the host response to N. meningitidis. While TLR4 has been suggested to play an important role in early containment of infection, the roles of TLR2 and TLR9 in meningococcal disease are not well described. Using a model for meningococcal sepsis, we report that TLR9?/? mice displayed reduced survival and elevated levels of bacteremia compared to wild-type mice. In contrast, TLR2?/? mice controlled the infection in a manner comparable to that of wild-type mice. TLR9 deficiency was also associated with reduced bactericidal activity in vitro, which was accompanied by reduced production of nitric oxide by TLR9-deficient macrophages. Interestingly, TLR9?/? mice recruited more macrophages to the bloodstream than wild-type mice and produced elevated levels of cytokines at late time points during infection. At the cellular level, activation of signal transduction and induction of cytokine gene expression were independent of TLR2 or TLR9 in macrophages and conventional dendritic cells. In contrast, plasmacytoid dendritic cells relied entirely on TLR9 to induce these activities. Thus, our data demonstrate an important role for TLR9 in host defense against N. meningitidis.
机译：脑膜炎奈瑟菌是脑膜炎和败血症的主要原因。脑膜炎球菌疾病的发病机制由细菌毒力因子和宿主的炎症反应决定。 Toll样受体（TLR）是炎症反应的主要激活因子，据报道TLR2，-4和-9参与了宿主对 N的反应。脑膜炎。尽管已建议TLR4在早期感染控制中起重要作用，但并未充分描述TLR2和TLR9在脑膜炎球菌疾病中的作用。使用脑膜炎球菌败血症模型，我们报道与野生型小鼠相比，TLR9 ？/？小鼠显示出降低的存活率和升高的菌血症水平。相反，TLR2 α/β小鼠以与野生型小鼠相当的方式控制感染。 TLR9缺乏症还与体外杀菌活性降低相关，并伴随着TLR9缺陷型巨噬细胞一氧化氮产生减少。有趣的是，与野生型小鼠相比，TLR9 α/β小鼠在血液中募集了更多的巨噬细胞，并且在感染过程中的较晚时间点产生了更高水平的细胞因子。在细胞水平上，巨噬细胞和常规树突状细胞中信号转导的激活和细胞因子基因表达的诱导独立于TLR2或TLR9。相反，浆细胞样树突状细胞完全依赖TLR9诱导这些活性。因此，我们的数据证明了TLR9在抗 N的宿主防御中的重要作用。脑膜炎。

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