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通过靶向病原体与共生体之间的相互作用来控制蜱虫媒介感染的类杆菌病。

Frankenbacteriosis targeting interactions between pathogen and symbiont to control infection in the tick vector.

作者信息

Mazuecos Lorena, Alberdi Pilar, Hernández-Jarguín Angélica, Contreras Marinela, Villar Margarita, Cabezas-Cruz Alejandro, Simo Ladislav, González-García Almudena, Díaz-Sánchez Sandra, Neelakanta Girish, Bonnet Sarah I, Fikrig Erol, de la Fuente José

机构信息

SaBio. Instituto de Investigación en Recursos Cinegéticos IREC-CSIC-UCLM-JCCM, Ronda de Toledo 12, 13005 Ciudad Real, Spain.

ANSES, INRAE, Ecole Nationale Vétérinaire d'Alfort, UMR BIPAR, Laboratoire de Santé Animale, 94700 Maisons-Alfort, France.

出版信息

iScience. 2023 Apr 18;26(5):106697. doi: 10.1016/j.isci.2023.106697. eCollection 2023 May 19.

DOI:10.1016/j.isci.2023.106697
PMID:37168564
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10165458/
Abstract

Tick microbiota can be targeted for the control of tick-borne diseases such as human granulocytic anaplasmosis (HGA) caused by model pathogen, . Frankenbacteriosis is inspired by Frankenstein and defined here as paratransgenesis of tick symbiotic/commensal bacteria to mimic and compete with tick-borne pathogens. Interactions between and symbiotic identified by metaproteomics analysis in midgut showed competition between both bacteria. Consequently, was selected for frankenbacteriosis for the control of infection and transmission. The results showed that Franken producing major surface protein 4 (MSP4) mimic pathogen and reduce infection in ticks by competition and interaction with cell receptor components of infection. Franken -MSP4 transovarial and trans-stadial transmission suggests that tick larvae with genetically modified Franken -MSP4 could be produced in the laboratory and released in the field to compete and replace the wildtype populations with associated reduction in pathogen infection/transmission and HGA disease risks.

摘要

蜱虫微生物群可作为控制蜱传疾病的靶点，如由模式病原体引起的人类粒细胞无形体病（HGA）。“弗兰肯细菌病”的灵感来源于《科学怪人》，在此被定义为蜱虫共生/共栖细菌的副转基因，以模仿并与蜱传病原体竞争。通过对蜱虫中肠的元蛋白质组学分析确定的[未提及具体细菌名称]与共生菌之间的相互作用表明，这两种细菌之间存在竞争。因此，[未提及具体细菌名称]被选为用于“弗兰肯细菌病”研究，以控制[未提及具体病原体名称]的感染和传播。结果表明，产生主要表面蛋白4（MSP4）的弗兰肯[未提及具体细菌名称]模仿病原体，并通过与感染的细胞受体成分竞争和相互作用来减少蜱虫中的感染。弗兰肯[未提及具体细菌名称]-MSP4的经卵和经发育阶段传播表明，在实验室中可以培育出带有转基因弗兰肯[未提及具体细菌名称]-MSP4的蜱虫幼虫，并将其释放到野外，以竞争并取代野生型种群，从而降低病原体感染/传播以及HGA疾病风险。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1873/10165458/06b5d4b92964/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1873/10165458/9ab5aedecd25/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1873/10165458/975265a9e0aa/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1873/10165458/1f4c954965b0/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1873/10165458/c0b517aa0039/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1873/10165458/ca259bf8ed5b/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1873/10165458/a8573340e7fe/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1873/10165458/1c41a189ea66/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1873/10165458/06b5d4b92964/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1873/10165458/9ab5aedecd25/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1873/10165458/975265a9e0aa/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1873/10165458/1f4c954965b0/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1873/10165458/c0b517aa0039/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1873/10165458/ca259bf8ed5b/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1873/10165458/a8573340e7fe/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1873/10165458/1c41a189ea66/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1873/10165458/06b5d4b92964/gr7.jpg

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