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【目的】阐明猪链球菌2型荚膜唾液酸是否影响细菌毒力以及宿主对其炎症反应应答,为研究猪链球菌2型的致病机制奠定基础。【方法】比较实验菌株对BLAB/c小鼠模型的致病性;通过涂板计数的方法检测实验菌株在小鼠体内的分布;观察小鼠脑组织病理改变,分析实验菌株感染小鼠后中枢神经系统的病变差异;从小鼠体外全血细胞水平,运用ELISA法检测实验菌株感染后细胞炎性因子的分泌水平。【结果】荚膜唾液酸合成基因neuB缺失突变株ΔneuB相比野生株05ZYH33株,对小鼠毒力显著降低,回复突变株cΔneuB毒力回复至野生株水平;野生株和突变株在血液及脑组织中分布具有显著差异,均可致BLAB/c小鼠脑组织不同程度的损伤;与野生株组相比较,细菌/细胞相互作用不同时间点后,突变株组体外刺激小鼠全血细胞分泌MCP-1、IL-6的水平显著提高;【结论】荚膜唾液酸影响细菌的毒力及宿主细胞对其的炎症反应应答,它是猪链球菌2型穿透血脑屏障导致脑膜炎的重要毒力因子。
【Objective】 To elucidate whether Streptococcus suis type 2 capsular sialic acid affects the virulence of bacteria and the host response to its inflammation, and lay the foundation for the study on the pathogenic mechanism of Streptococcus suis type 2. 【Method】 The pathogenicity of the experimental strains to the BLAB / c mouse model was compared. The distribution of the experimental strains in the mice was detected by the method of plate counting. The histopathological changes of the mice were observed. The pathological changes of the nervous system were observed. The levels of inflammatory cytokines in the infected mice were detected by ELISA from the level of whole blood cells in vitro. 【Results】 The results showed that the virulence of neuB-deficient mutant neuB in capsular sialic acid was significantly lower than that of wild-type strain 05ZYH33, and the virulence of cΔneuB was restored to wild-type strain. There were significant differences in the distribution of the tissue, can cause BLAB / c mouse brain tissue injury to varying degrees; compared with the wild-type group, bacterial / cell interaction at different time points, the mutant group stimulated mouse whole blood cells to secrete MCP -1 and IL-6. 【Conclusion】 Capsular sialic acid affects the virulence of bacteria and the response of host cells to the inflammatory response. It is important for Streptococcus suis type 2 to penetrate the blood-brain barrier to cause meningitis Virulence factors.