4D label-free proteomic analysis reveals key potential pathways of Toxoplasma invasion into the central nervous system
文献类型： 外文期刊
作者： Ren, Zhaowen 1 ; Yang, Zipeng 1 ; Yuan, Hao 1 ; Song, Yining 1 ; He, Houjing 1 ; Nie, Linchong 1 ; Wang, Xiaohu 2 ; Yuan, Zi-Guo 1 ; Zhang, Xiu-Xiang 1 ;
作者机构： 1.South China Agr Univ, Coll Vet Med, Key Lab Zoonosis Prevent & Control Guangdong Prov, Guangzhou, Guangdong, Peoples R China
2.Guangdong Acad Agr Sci, Key Lab Livestock Dis Prevent Guangdong Prov, Key Lab Avian Influenza & Other Major Poultry Dis, Inst Anim Hlth,Minist Agr & Rural Affairs, Wushan St, Guangzhou 510640, Peoples R China
3.Guangdong Acad Agr Sci, Inst Anim Hlth, Key Lab Prevent & Control Avian Influenza & Other, Minist Agr & Rural Affairs, Wushan St, Guangzhou 510640, Peoples R China
关键词： 4D label-free; Toxoplasma gondii; Brain proteome; Pathogen-host interaction
期刊名称：INTERNATIONAL IMMUNOPHARMACOLOGY （ 影响因子：4.8； 五年影响因子：5.0 ）
ISSN： 1567-5769
年卷期： 2024 年 138 卷
页码：
收录情况： SCI
摘要： Toxoplasma gondii is a successful parasite capable of infecting a wide range of warm-blooded animals, including people, livestock, and wildlife. In individuals with intact immune function, T. gondii can invade the host brain tissue by altering the blood-brain barrier permeability, leading to chronic infection. Proteins play crucial regulatory roles in disease progression. By monitoring changes in proteins, a deeper understanding of the molecular mechanisms underlying host resistance to infection and the potential pathogenic mechanisms of pathogens can be gained. This study analyzed differential protein expression and associated signaling pathways in mouse brain tissues during acute and chronic T. gondii infection using proteomic and bioinformatics methods. The results showed that during acute and chronic T. gondii infection stages, 74 and 498 differentially expressed proteins (DEPs) were identified in mouse brain tissue, respectively. Among them, 45 and 309 were up-regulated, while 29 and 189 were down-regulated. GO and KEGG analyses revealed that some of these DEPs were implicated in host immunity, pathogen immune evasion, and T. gondii invasion of the central nervous system, particularly interleukin production and secretion, complement system activation, and alterations in tight junction pathways. Notably, the upregulation of Rab13 was identified as a potential molecular mechanism for T. gondii to regulate blood-brain barrier permeability and facilitate central nervous system invasion. Our findings provided fundamental data for understanding host control of Toxoplasmosis infection and offered new insights into parasite immune evasion and invasion mechanisms within the central nervous system. These insights are crucial for developing strategies to prevent the establishment of chronic T. gondii infection.
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