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蛋白 Tp0136 促进血管生成，以促进的传播。

protein Tp0136 promotes angiogenesis to facilitate the dissemination of .

机构信息

Center of Clinical Laboratory, Zhongshan Hospital Xiamen University, School of Medicine, Xiamen University, Xiamen, People's Republic of China.

Institute of Infectious Disease, School of Medicine, Xiamen University, Xiamen, People's Republic of China.

出版信息

Emerg Microbes Infect. 2024 Dec;13(1):2382236. doi: 10.1080/22221751.2024.2382236. Epub 2024 Aug 2.

DOI:10.1080/22221751.2024.2382236
PMID:39017656
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11299452/
Abstract

The incompletely eliminated () during primary syphilis chancre infection can result in the progression of secondary, tertiary, or latent syphilis in individuals, suggesting that has successfully evaded the immune response and spread to distant sites. The mechanism underlying the dissemination of is unclear. Here, a syphilitic rabbit model dorsal-injected with recombinant Tp0136 protein or Tp0136 antibody subcutaneously was used to demonstrate the role of Tp0136 protein in promoting the dissemination of to the testis and angiogenesis ; vascular endothelial cell line HMEC-1 was employed to display that Tp0136 protein enhances the angiogenesis. Furthermore, the three-dimensional microfluidic angiogenesis system showed that the angiogenesis would heighten vascular permeability. Then transcriptome sequencing analysis, in conjunction with cell-level validation, elucidated the critical role of the PI3K-AKT signaling pathway in the promotion of angiogenesis by Tp0136 protein, resulting in heightened permeability. These findings elucidate the strategy employed by in evading immune clearance.

摘要

在一期梅毒硬下疳感染中未完全清除的梅毒螺旋体（）可能导致个体发生二期、三期或潜伏梅毒，这表明梅毒螺旋体成功地逃避了免疫反应并扩散到远处。梅毒螺旋体传播的机制尚不清楚。在这里，我们使用背部注射重组 Tp0136 蛋白或 Tp0136 抗体的梅毒兔模型，证明了 Tp0136 蛋白在促进梅毒螺旋体向睾丸和血管生成传播中的作用；使用血管内皮细胞系 HMEC-1 显示 Tp0136 蛋白增强了血管生成。此外，三维微流控血管生成系统表明，血管生成会增加血管通透性。然后，转录组测序分析结合细胞水平验证，阐明了 PI3K-AKT 信号通路在 Tp0136 蛋白促进血管生成和增加通透性中的关键作用。这些发现阐明了梅毒螺旋体逃避免疫清除的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8393/11299452/63925f99a090/TEMI_A_2382236_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8393/11299452/a5668f819142/TEMI_A_2382236_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8393/11299452/7bfd024a799f/TEMI_A_2382236_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8393/11299452/42093903bf64/TEMI_A_2382236_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8393/11299452/01c239b7e8db/TEMI_A_2382236_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8393/11299452/12fef47d9033/TEMI_A_2382236_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8393/11299452/63925f99a090/TEMI_A_2382236_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8393/11299452/a5668f819142/TEMI_A_2382236_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8393/11299452/7bfd024a799f/TEMI_A_2382236_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8393/11299452/42093903bf64/TEMI_A_2382236_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8393/11299452/01c239b7e8db/TEMI_A_2382236_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8393/11299452/12fef47d9033/TEMI_A_2382236_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8393/11299452/63925f99a090/TEMI_A_2382236_F0006_OC.jpg

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Treponema pallidum recombinant protein Tp47 enhanced interleukin-6 secretion in human dermal fibroblasts through the toll-like receptor 2 via the p38, PI3K/Akt, and NF-κB signalling pathways.梅毒螺旋体重组蛋白Tp47通过Toll样受体2，经由p38、PI3K/Akt和NF-κB信号通路增强人皮肤成纤维细胞中白细胞介素-6的分泌。
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Genome Biol. 2023 Apr 21;24(1):87. doi: 10.1186/s13059-023-02931-y.
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