Analysis on pathogenic mechanism of fish pathogen Edwardsiella tarda

鱼类病原菌迟缓爱德华氏菌致病机制分析

基本信息

批准号：
18580184
负责人：
OKUDA Jun
金额：
$ 2.35万
依托单位：
Kyoto Pharmaceutical University (2007)Hiroshima University (2006)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2006
资助国家：
日本
起止时间：
2006 至 2007
项目状态：
已结题

项目摘要

(1) Intracellular replication of Edwardsiella tarda in murine macrophage is dependent on the type III secretion systemEdwardsiella tarda is a pathogen with a broad host range that infects both animals and humans. Resistance to phagocytic killing may be involved in the pathogenicity of this bacterium. We showed that intracellular replication of E. tarda in murine macrophages is dependent on the type III secretion system and induces an anti-apoptotic effect by up-regulating anti-apoptotic NF-kappaB target genes. The wild-type strain replicates within the phagosomal membrane of macrophages ; whereas the type III mutant does not.(2) Microarray analysisMicroarray analysis shows the mRNA expression level of NF-kappaB target genes (e.g. pro-inflammatory cytokines and anti-apoptotic genes) in macrophages infected with the wild-type strain were up-regulated compared to macrophages infected with the type III mutant. Up-regulation of anti-apoptotic NF-kappaB target genes is responsible for the an … More ti-apoptotic activity of E. tarda and is required for intracellular replication in murine macrophages(3) The type III secretion system-dependent repression of NF-kappaB activation to the intracellular growth of Edwardsiella tarda in human epithelial cellsWe next showed that the TTSS is also needed for intracellular growth of the bacterium in human epithelial cells (Hep-2). However, different from the previous microarray analyses on murine macrophages, upregulation of the mRNA expression level of NF-kappaB target genes was not detected in the infected Hep-2 cells. The wild-type E tarda, but not its TTSS mutant, actually repressed the tumor necrosis factor alpha-dependent NF-kappaB activation in an NF-kappaB reporter gene assay. These results suggest TTSS-dependent repression of the NF-kappaB activation in Hep-2 cells infected with E. tarda.Taken together, these results suggest that drug or vaccine specifically targeting the type III secretion system of this bacterium may contribute to decreasing the industrial loss caused by E. tarda infection to cultured fish such as red sea bream and Japanese flounder. Less

(1)迟缓爱德华氏菌在小鼠巨噬细胞中的细胞内复制依赖于III型分泌系统迟缓爱德华氏菌是一种宿主范围广泛的病原体，其对吞噬杀伤的抵抗力可能与该细菌的致病性有关。 E. tarda 在小鼠巨噬细胞中的细胞内复制依赖于 III 型分泌系统，并通过以下方式诱导抗凋亡作用上调抗凋亡NF-kappaB靶基因。野生型菌株在巨噬细胞的吞噬体膜内复制；而III型突变体则不然。(2)微阵列分析微阵列分析显示NF-kappaB靶基因的mRNA表达水平。与感染 III 型菌株的巨噬细胞相比，感染野生型菌株的巨噬细胞中的促炎细胞因子和抗凋亡基因）上调抗凋亡 NF-kappaB 靶基因的上调是 E. tarda 的抗凋亡活性的原因，并且是小鼠巨噬细胞内细胞内复制所必需的 (3) III 型分泌系统依赖性抑制NF-κB 激活对人上皮细胞中迟缓爱德华氏菌的细胞内生长我们接下来表明，TTSS 也是该细菌在人体内的细胞内生长所必需的然而，与之前对小鼠巨噬细胞的微阵列分析不同，在感染的Hep-2细胞中未检测到NF-kappaB靶基因的mRNA表达水平的上调。但它的 TTSS 突变体实际上在 NF-kappaB 报告基因测定中抑制了肿瘤坏死因子 α 依赖性 NF-kappaB 激活。这些结果表明 TTSS 依赖性抑制。感染 E. tarda 的 Hep-2 细胞中 NF-kappaB 激活。总之，这些结果表明，专门针对该细菌的 III 型分泌系统的药物或疫苗可能有助于减少 E. tarda 感染对培养物造成的工业损失。鲷鱼、比目鱼等鱼类较少。

项目成果

期刊论文数量（0）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Isolation and characterization of bacteria from the copepod Pseudocaligus fugu ectoparasitic on the panther puffer Takifugu pardalis with the emphasis on TTX

体外寄生在豹鲀 Takifugu pardalis 上的桡足类 Pseudocaligus fugu 细菌的分离和表征，重点是 TTX

DOI：
发表时间：
2007
期刊：
影响因子：
0
作者：
Venmathi Maran B.A.; E.Iwamoto; J.Okuda; S.Matsuda; S.Taniyama; Y.Shida; M.Asakawa; S.Ohtsuka; T.Nakai;G.A.Boxshall
通讯作者：
G.A.Boxshall

Sodium choloride-enhanced adherence of Edwardsiella tarda to HEp-2 cells.

氯化钠增强迟缓爱德华氏菌对 HEp-2 细胞的粘附。