Brucella requires a functional Type IV secretion system to elicit innate immune responses in mice
Brucella requires a functional Type IV secretion system to elicit innate immune responses in mice
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DOI：
10.1111/j.1462-5822.2007.00922.x
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发表时间：
2007-07-01
影响因子：
3.4
通讯作者：
Tsolis, Renee M.
中科院分区：
文献类型：
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作者：
Roux, Christelle M.;Rolan, Hortensia G.;Tsolis, Renee M.
virB 操纵子编码 IV 型分泌系统 (T4SS)，对于布鲁氏菌属的细胞内存活和持续感染至关重要。为了更好地了解 T4SS 在逃避宿主防御机制和建立慢性感染中的作用，我们比较了宿主对野生型和 virB 突变布鲁氏菌菌株感染的反应的转录谱。接种野生型布鲁氏菌菌株三天后，对小鼠脾细胞的基因表达谱进行分析，发现炎症反应，由 I 型和 II 型干扰素诱导的基因显着上调。实时 RT-PCR 显示，这些途径中的一组基因在感染后第 3 天被诱导，并在第 7 天下降到基线水平。相比之下，两种 virB 突变株均未引发促炎基因表达谱，表明需要 T4SS 来触发这种反应。使用 I 型干扰素受体敲除小鼠进行的感染研究表明，I 型干扰素信号传导的缺乏不会影响感染前 4 周内布鲁氏菌的复制。因此，I 型干扰素的诱导似乎并不是 T4SS 促进布鲁氏菌持续感染的重要机制。
The virB operon, encoding a Type IV secretion system (T4SS), is essential for intracellular survival and persistent infection by Brucella spp. To better understand the role of the T4SS in evading host defence mechanisms and establishing chronic infection, we compared transcriptional profiles of the host response to infection with wild-type and virB mutant Brucella strains. Analysis of gene expression profiles in murine splenocytes 3 days after inoculation with wild-type Brucella strains revealed an inflammatory response, with a prominent upregulation of genes induced by both type I and type II interferons. Real-time RT-PCR showed that a group of genes from these pathways were induced by day 3 post infection and declined to baseline levels by day 7. In contrast, neither of the two virB mutant strains elicited a proinflammatory gene expression profile, demonstrating that the T4SS was required to trigger this response. Infection studies using type I interferon receptor knockout mice showed that a lack of type I interferon signalling did not affect Brucella replication during the first 4 weeks of infection. Thus, induction of type I interferons does not appear to be an essential mechanism by which the T4SS promotes persistent infection by Brucella.