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脂类在:宿主依赖性和毒力因子。

Lipids in : Host-Dependence and Virulence Factors.

机构信息

College of Sciences and Humanities, Autonomous University of Mexico City, Mexico City, Mexico.

BioImage Analysis Unit, Pasteur Institute, Paris, France.

出版信息

Front Cell Infect Microbiol. 2020 Mar 10;10:75. doi: 10.3389/fcimb.2020.00075. eCollection 2020.

DOI:10.3389/fcimb.2020.00075
PMID:32211340
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7075943/
Abstract

Lipids are essential players in parasites pathogenesis. In particular, the highly phagocytic trophozoites of , the causative agent of amoebiasis, exhibit a dynamic membrane fusion and fission, in which lipids strongly participate; particularly during the overstated motility of the parasite to reach and attack the epithelia and ingest target cells. Synthesis and metabolism of lipids in this protozoan present remarkable difference with those performed by other eukaryotes. Here, we reviewed the current knowledge on lipids in . Trophozoites synthesize phosphatidylcholine and phosphatidylethanolamine by the Kennedy pathway; and sphingolipids, phosphatidylserine, and phosphatidylinositol, by processes similar to those used by other eukaryotes. However, trophozoites lack enzymes for cholesterol and fatty acids synthesis, which are scavenged from the host or culture medium by specific mechanisms. Cholesterol, a fundamental molecule for the expression of virulence, is transported from the medium into the trophozoites by EhNPC1 and EhNPC2 proteins. Inside cells, lipids are distributed by different pathways, including by the participation of the endosomal sorting complex required for transport (ESCRT), involved in vesicle fusion and fission. Cholesterol interacts with the phospholipid lysobisphosphatidic acid (LBPA) and EhADH, an ALIX family protein, also involved in phagocytosis. In this review, we summarize the known information on phospholipids synthesis and cholesterol transport as well as their metabolic pathways in ; highlighting the mechanisms used by trophozoites to dispose lipids involved in the virulence processes.

摘要

脂质是寄生虫发病机制中的重要参与者。特别是引起阿米巴病的病原体,其吞噬能力很强的滋养体表现出动态的膜融合和裂变,脂质在其中强烈参与;特别是在寄生虫过度运动以到达和攻击上皮细胞并摄取靶细胞时。这种原生动物的脂质合成和代谢与其他真核生物有显著的不同。在这里,我们综述了关于的脂质的现有知识。滋养体通过 Kennedy 途径合成磷脂酰胆碱和磷脂酰乙醇胺;通过类似于其他真核生物使用的过程合成鞘脂、磷脂酰丝氨酸和磷脂酰肌醇。然而,滋养体缺乏胆固醇和脂肪酸合成所需的酶,这些酶通过特定的机制从宿主或培养基中摄取。胆固醇是表达毒力的基本分子,通过 EhNPC1 和 EhNPC2 蛋白从培养基中转运到滋养体中。在细胞内,脂质通过不同的途径分布,包括参与囊泡融合和裂变的内体分选复合物所需的运输 (ESCRT)。胆固醇与磷脂酰肌醇磷酸二酰甘油 (LBPA) 和 EhADH 相互作用,EhADH 是一种参与吞噬作用的 ALIX 家族蛋白。在这篇综述中,我们总结了关于磷脂合成和胆固醇运输及其在中的代谢途径的已知信息,强调了滋养体用于处理与毒力过程相关的脂质的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e19a/7075943/8b5a2d39d595/fcimb-10-00075-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e19a/7075943/8b5a2d39d595/fcimb-10-00075-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e19a/7075943/8b5a2d39d595/fcimb-10-00075-g0001.jpg

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