弓形虫感染会误导胎盘滋养层细胞系的分化

Leah F. Cabo, Liheng Yang, Mingze Gao, Rafaela J. da Silva, NyJaee N. Washington, Sarah M. Reilly, Christina J. Megli, Carolyn B. Coyne, Jon P. Boyle
{"title":"弓形虫感染会误导胎盘滋养层细胞系的分化","authors":"Leah F. Cabo, Liheng Yang, Mingze Gao, Rafaela J. da Silva, NyJaee N. Washington, Sarah M. Reilly, Christina J. Megli, Carolyn B. Coyne, Jon P. Boyle","doi":"10.1101/2024.09.10.612241","DOIUrl":null,"url":null,"abstract":"Pregnancy is a critical point of vulnerability to infection and other insults that could compromise proper fetal development. The placenta acts as a protective and nutrient-permeable barrier to most infectious agents, but a few are capable of bypassing its defenses. Remarkably little is known about how exposure to these select pathogens might impact ongoing placental development. Here we demonstrate that <em>Toxoplasma gondii</em> entirely misdirects the developmental program of trophoblast stem cells. Infection of progenitor cytotrophoblasts prevents fusion and differentiation to infection-resistant syncytiotrophoblast. Rather, <em>T. gondii</em> elicits a unique transcriptional identity that polarizes cytotrophoblasts to the infection-permissive extravillous trophoblast fate. Strong evidence of developmental disruption is found in multiple orthogonal models, including trophoblast stem cells, trophoblast organoids, and chorionic villi. Manipulation of cell fate by the parasite is most dramatic in trophoblast organoids, where we see robust outgrowth of HLA-G(+) extravillous trophoblasts. Collectively, these data show that <em>Toxoplasma</em> antagonizes differentiation of an infection-resistant cell type by inducing formation of an infection-permissive cell type, therefore potentiating its own transmission to the fetus.","PeriodicalId":501269,"journal":{"name":"bioRxiv - Developmental Biology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Toxoplasma gondii infection misdirects placental trophoblast lineage specification\",\"authors\":\"Leah F. Cabo, Liheng Yang, Mingze Gao, Rafaela J. da Silva, NyJaee N. Washington, Sarah M. Reilly, Christina J. Megli, Carolyn B. Coyne, Jon P. Boyle\",\"doi\":\"10.1101/2024.09.10.612241\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Pregnancy is a critical point of vulnerability to infection and other insults that could compromise proper fetal development. The placenta acts as a protective and nutrient-permeable barrier to most infectious agents, but a few are capable of bypassing its defenses. Remarkably little is known about how exposure to these select pathogens might impact ongoing placental development. Here we demonstrate that <em>Toxoplasma gondii</em> entirely misdirects the developmental program of trophoblast stem cells. Infection of progenitor cytotrophoblasts prevents fusion and differentiation to infection-resistant syncytiotrophoblast. Rather, <em>T. gondii</em> elicits a unique transcriptional identity that polarizes cytotrophoblasts to the infection-permissive extravillous trophoblast fate. Strong evidence of developmental disruption is found in multiple orthogonal models, including trophoblast stem cells, trophoblast organoids, and chorionic villi. Manipulation of cell fate by the parasite is most dramatic in trophoblast organoids, where we see robust outgrowth of HLA-G(+) extravillous trophoblasts. Collectively, these data show that <em>Toxoplasma</em> antagonizes differentiation of an infection-resistant cell type by inducing formation of an infection-permissive cell type, therefore potentiating its own transmission to the fetus.\",\"PeriodicalId\":501269,\"journal\":{\"name\":\"bioRxiv - Developmental Biology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-09-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"bioRxiv - Developmental Biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1101/2024.09.10.612241\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"bioRxiv - Developmental Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1101/2024.09.10.612241","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

妊娠期是胎儿容易受到感染和其他损伤的关键时期,这些损伤可能会影响胎儿的正常发育。胎盘对大多数感染性病原体起着保护和营养渗透屏障的作用,但也有少数病原体能够绕过胎盘的防御。对于接触这些特定病原体会如何影响胎盘的持续发育,人们知之甚少。在这里,我们证明弓形虫会完全误导滋养层干细胞的发育程序。原代滋养细胞受到感染后会阻止融合和分化为抗感染的合胞滋养细胞。相反,淋球菌会引起一种独特的转录特性,将滋养细胞极化为允许感染的滋养外细胞。在滋养层干细胞、滋养层有机体和绒毛等多个正交模型中都发现了发育中断的有力证据。寄生虫对细胞命运的操纵在滋养层有机体中最为显著,我们在其中看到了HLA-G(+)外滋养层滋养细胞的强劲生长。总之,这些数据表明弓形虫通过诱导形成允许感染的细胞类型来拮抗抗感染细胞类型的分化,从而增强其自身向胎儿的传播。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Toxoplasma gondii infection misdirects placental trophoblast lineage specification
Pregnancy is a critical point of vulnerability to infection and other insults that could compromise proper fetal development. The placenta acts as a protective and nutrient-permeable barrier to most infectious agents, but a few are capable of bypassing its defenses. Remarkably little is known about how exposure to these select pathogens might impact ongoing placental development. Here we demonstrate that Toxoplasma gondii entirely misdirects the developmental program of trophoblast stem cells. Infection of progenitor cytotrophoblasts prevents fusion and differentiation to infection-resistant syncytiotrophoblast. Rather, T. gondii elicits a unique transcriptional identity that polarizes cytotrophoblasts to the infection-permissive extravillous trophoblast fate. Strong evidence of developmental disruption is found in multiple orthogonal models, including trophoblast stem cells, trophoblast organoids, and chorionic villi. Manipulation of cell fate by the parasite is most dramatic in trophoblast organoids, where we see robust outgrowth of HLA-G(+) extravillous trophoblasts. Collectively, these data show that Toxoplasma antagonizes differentiation of an infection-resistant cell type by inducing formation of an infection-permissive cell type, therefore potentiating its own transmission to the fetus.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
The pericardium forms as a distinct structure during heart formation Centralspindlin promotes C. elegans anchor cell specification, vulva induction and morphogenesis Human macula formation involves two waves of retinoic acid signaling suppression via CYP26A1 regulating cell cycle exit and cone specification Single Cell Profiling in the Sox10Dom/+ Hirschsprung Mouse Implicates Hoxa6 in Enteric Neuron Lineage Allocation Mylpf dosage is proportionate to fast-twitch myofibril size in the zebrafish embryo
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1