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迟缓爱德华氏菌的铁辅因子超氧化物歧化酶抑制巨噬细胞介导的固有免疫反应。

The iron-cofactored superoxide dismutase of Edwardsiella tarda inhibits macrophage-mediated innate immune response.

机构信息

Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, PR China.

出版信息

Fish Shellfish Immunol. 2010 Dec;29(6):972-8. doi: 10.1016/j.fsi.2010.08.004. Epub 2010 Aug 21.

Abstract

Edwardsiella tarda is a Gram-negative bacterium that can infect a wide variety of marine and freshwater fish and cause severe economic losses worldwide. With an aim to elucidate the virulence mechanism of E. tarda, we in this study cloned and analyzed the function of an iron-cofactored superoxide dismutase (FeSOD) from a pathogenic E. tarda strain TX01 isolated from diseased fish. FeSOD is 192-residue in length and contains domain structures that are conserved among iron/manganese superoxide dismutases. Recombinant FeSOD purified from Escherichia coli exhibits apparent superoxide dismutase activity. Quantitative real-time RT-PCR analysis indicated that FeSOD expression is significantly upregulated immediately following TX01 infection of Japanese flounder (Paralichthys olivaceus) head kidney (HK) macrophages and cultured FG cells. Compared to the wild type strain TX01, the FeSOD mutant strain TXSod is (i) more sensitive to H(2)O(2)-induced oxidative damage, (ii) less resistant against serum- and macrophage-mediated bacterial killing, (iii) significantly weakened in the ability to invade into FG cells and to disseminate in fish blood and liver, and (iv) deficient in blocking macrophage respiratory burst activity and production of reactive oxygen species. Furthermore, HK macrophages infected by TXSod exhibits significantly increased expression of inflammatory cytokines compared to macrophages infected by TX01. Taken together, these results indicate that FeSOD is a virulence factor that plays an important role in the pathogenicity of E. tarda by inhibiting macrophage-mediated innate immune response.

摘要

迟缓爱德华氏菌是一种革兰氏阴性细菌,能够感染多种海水和淡水鱼类,并在全球范围内造成严重的经济损失。本研究旨在阐明迟缓爱德华氏菌的毒力机制,我们克隆并分析了从患病鱼类中分离的致病性迟缓爱德华氏菌菌株 TX01 的一种含铁辅因子超氧化物歧化酶(FeSOD)的功能。FeSOD 长度为 192 个残基,含有铁/锰超氧化物歧化酶中保守的结构域。从大肠杆菌中纯化的重组 FeSOD 表现出明显的超氧化物歧化酶活性。定量实时 RT-PCR 分析表明,FeSOD 的表达在 TX01 感染日本牙鲆(Paralichthys olivaceus)头肾(HK)巨噬细胞和培养的 FG 细胞后立即显著上调。与野生型菌株 TX01 相比,FeSOD 突变菌株 TXSod (i)对 H₂O₂诱导的氧化损伤更敏感,(ii)对血清和巨噬细胞介导的细菌杀伤的抗性降低,(iii)在入侵 FG 细胞和在鱼血液和肝脏中扩散的能力显著减弱,(iv)在阻断巨噬细胞呼吸爆发活性和产生活性氧的能力缺失。此外,与感染 TX01 的巨噬细胞相比,感染 TXSod 的 HK 巨噬细胞中炎症细胞因子的表达显著增加。总之,这些结果表明 FeSOD 是一种毒力因子,通过抑制巨噬细胞介导的固有免疫反应,在迟缓爱德华氏菌的致病性中发挥重要作用。

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