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首页> 外文期刊>Infection and immunity >The Type VI Secretion System Plays a Role in Type 1 Fimbria Expression and Pathogenesis of an Avian Pathogenic Escherichia coli Strain
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The Type VI Secretion System Plays a Role in Type 1 Fimbria Expression and Pathogenesis of an Avian Pathogenic Escherichia coli Strain

机译:VI型分泌系统在禽病原性大肠杆菌株的1型菌毛表达和发病机理中发挥作用。

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Avian pathogenic Escherichia coli (APEC) strains frequently cause extraintestinal infections and are responsible for significant economic losses in the poultry industry worldwide. APEC isolates are closely related to human extraintestinal pathogenic E. coli (ExPEC) strains and may also act as pathogens for humans. Known APEC virulence factors include adhesins such as type 1 fimbriae and curli, iron acquisition systems, and cytotoxins. Here we show that APEC strain SEPT362, isolated from a septicemic hen, expresses a type VI secretion system (T6SS); causes cytoskeleton rearrangements; and invades epithelial cells, replicates within macrophages, and causes lethal disease in chicks. To assess the contribution of the T6SS to SEPT362 pathogenesis, we generated two mutants, hcp (which encodes a protein suggested to be both secreted and a structural component of the T6SS) and clpV (encoding the T6SS ATPase). Both mutants showed decreased adherence and actin rearrangement on epithelial cells. However, only the hcp mutant presented a mild decrease in its ability to invade epithelial cells, and none of these mutants were defective for intramacrophage replication. Transcriptome studies showed that the level of expression of type 1 fimbriae was decreased in these mutants, which may account for the diminished adhesion and invasion of epithelial cells. The T6SS seems to be important for the disease process, given that both mutants were attenuated for infection in chicks. These results suggest that the T6SS influences the expression of type 1 fimbriae and contributes to APEC pathogenesis.
机译:禽致病性大肠埃希菌(APEC)菌株经常引起肠外感染,并造成全球家禽业的重大经济损失。 APEC分离株与人肠外致病性大肠杆菌(ExPEC)菌株密切相关,也可能充当人类的病原体。已知的APEC毒力因子包括粘附素,例如1型菌毛和卷曲菌,铁捕获系统和细胞毒素。在这里,我们显示从败血病母鸡中分离出的APEC株SEPT362表达VI型分泌系统(T6SS);引起细胞骨架重排;并侵入上皮细胞,在巨噬细胞内复制,并导致雏鸡致死性疾病。为了评估T6SS对SEPT362发病机制的贡献,我们生成了两个突变体,hcp(编码被认为是分泌的蛋白质和T6SS的结构成分)和clpV(编码T6SS ATPase)。两种突变体均显示上皮细胞的粘附和肌动蛋白重排减少。但是,只有hcp突变体侵袭上皮细胞的能力出现了轻度下降,而且这些突变体均无巨噬细胞内复制缺陷。转录组研究表明,这些突变体中1型菌毛的表达水平降低,这可能是上皮细胞粘附和侵袭减少的原因。 T6SS对于疾病过程似乎很重要,因为这两个突变体都因鸡的感染而减毒。这些结果表明,T6SS影响1型菌毛的表达并有助于APEC发病机理。

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