The autotransporter BafA contributes to the proangiogenic potential of <i>Bartonella elizabethae</i>

The autotransporter BafA contributes to the proangiogenic potential of <i>Bartonella elizabethae</i>
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自转运蛋白 BafA 有助于<i>伊丽莎白巴尔通体</i>的促血管生成潜力

DOI:
10.1111/1348-0421.13057
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发表时间:
2023
影响因子:
2.6
通讯作者:
Tsukamoto Kentaro
Tsukamoto Kentaro
中科院分区:
医学4区
文献类型:
--
作者:
Suzuki Natsumi;Kumadaki Kayo;Tatematsu Kaoru;Doi Yohei;Tsukamoto Kentaro

文献摘要

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巴尔通体是一种由老鼠传播的人畜共患病细菌,可引起人类感染性心内膜炎或神经视网膜炎。最近,报道了一例由这种细菌引起的细菌性血管瘤病(BA),这导致了对B。伊利沙伯可能还会引发血管增殖。然而,目前还没有关于B的报道。伊利沙伯能促进人血管内皮细胞的增殖或血管生成,到目前为止,这种细菌对血管内皮细胞的影响尚不清楚。我们最近发现了一种促血管生成的自身转运蛋白,BAFA,它是由B分泌的。母鸡和B。Quintana,它们被认为是Bartonellaspp.对人类的BA负责。在这里,我们假设B。Elizabthae还含有功能性的bafA基因,并检测了重组B的促血管生成活性。伊利沙贝亚科的BAFA。BafAgene of B.与BAFA OFB的氨基酸序列同源性为51.1%。母鸡占52.5%。Quintanain位于基因组的同线区域。重组蛋白OfB的N端客体结构域。Eizabthae-BAFA促进EC的增殖和毛细血管结构的形成。此外,正如INB观察到的那样,它上调了血管内皮生长因子的受体信号通路。亨塞莱-BAFA。综上所述,白僵菌来源的BAFA刺激人EC增殖,并可能有助于该细菌的血管生成潜能。到目前为止,在所有引起BA的Bartonellasp.中都发现了功能性的bafA基因,支持BAFA在BA的发病机制中可能发挥的关键作用。
Bartonella elizabethaeis a rat‐borne zoonotic bacterium that causes human infectious endocarditis or neuroretinitis. Recently, a case of bacillary angiomatosis (BA) resulting from this organism was reported, leading to speculation thatB. elizabethaemay also trigger vasoproliferation. However, there are no reports ofB. elizabethaepromoting human vascular endothelial cell (EC) proliferation or angiogenesis, and to date, the effects of this bacterium on ECs are unknown. We recently identified a proangiogenic autotransporter, BafA, secreted fromB. henselaeandB. quintana, which are recognized asBartonellaspp. responsible for BA in humans. Here, we hypothesized thatB. elizabethaealso harbored a functionalbafAgene and examined the proangiogenic activity of recombinantB. elizabethae–derived BafA. ThebafAgene ofB. elizabethae, which was found to share a 51.1% amino acid sequence identity with BafA ofB. henselaeand 52.5% with that ofB. quintanain the passenger domain, was located in a syntenic region of the genome. The recombinant protein of the N‐terminal passenger domain ofB. elizabethae‐BafA facilitated EC proliferation and capillary structure formation. Furthermore, it upregulated the receptor signaling pathway of vascular endothelial growth factor, as observed inB. henselae‐BafA. Taken together,B. elizabethae–derived BafA stimulates human EC proliferation and may contribute to the proangiogenic potential of this bacterium. So far, functionalbafAgenes have been found in all BA‐causingBartonellaspp., supporting the key role BafA may play in BA pathogenesis.