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米替福新敏感和米替福新耐药利什曼原虫的比较转录表达分析。

Comparative transcript expression analysis of miltefosine-sensitive and miltefosine-resistant Leishmania donovani.

机构信息

National Institute of Pathology (ICMR), Safdarjung Hospital Campus, New Delhi, 110029, India.

出版信息

Parasitol Res. 2014 Mar;113(3):1171-84. doi: 10.1007/s00436-014-3755-6. Epub 2014 Jan 22.

Abstract

Leishmania donovani is the causative agent of anthroponotic visceral leishmaniasis in the Indian subcontinent. Oral miltefosine therapy has recently replaced antimonials in endemic areas. However, the drug is at risk of emergence of resistance due to unrestricted use, and, already, there are indications towards decline in treatment efficacy. Hence, understanding the mechanism of miltefosine resistance in the parasite is crucial. We employed genomic microarray analysis to compare the gene expression patterns of miltefosine-resistant and miltefosine-sensitive L. donovani. Three hundred eleven genes, representing ∼3.9% of the total Leishmania genome, belonging to various functional categories including metabolic pathways, transporters, and cellular components, were differentially expressed in miltefosine-resistant parasite. Results in the present study highlighted the probable mechanisms by which the parasite sustains miltefosine pressure including (1) compromised DNA replication/repair mechanism, (2) reduced protein synthesis and degradation, (3) altered energy utilization via increased lipid degradation, (4) increased ABC 1-mediated drug efflux, and (5) increased antioxidant defense mechanism via elevated trypanothione metabolism. The study provided the comprehensive insight into the underlying mechanism of miltefosine resistance in L. donovani that may be useful to design strategies to increase lifespan of this important oral antileishmanial drug.

摘要

杜氏利什曼原虫是印度次大陆人类内脏利什曼病的病原体。口服米替福新治疗最近已取代了在流行地区使用的锑剂。然而,由于不受限制的使用,该药物有出现耐药性的风险,并且已经有迹象表明治疗效果正在下降。因此,了解寄生虫对米替福新耐药的机制至关重要。我们采用基因组微阵列分析比较了米替福新耐药和米替福新敏感的杜氏利什曼原虫的基因表达模式。311 个基因,代表总利什曼原虫基因组的约 3.9%,属于各种功能类别,包括代谢途径、转运蛋白和细胞成分,在米替福新耐药寄生虫中差异表达。本研究的结果强调了寄生虫维持米替福新压力的可能机制,包括(1)受损的 DNA 复制/修复机制,(2)减少蛋白质合成和降解,(3)通过增加脂质降解来改变能量利用,(4)通过增加 ABC1 介导的药物外排来增加 ABC1 介导的药物外排,以及(5)通过提高三肽硫醇代谢来增加抗氧化防御机制。该研究深入了解了杜氏利什曼原虫对米替福新耐药的潜在机制,这可能有助于设计策略来延长这种重要的口服抗利什曼原虫药物的寿命。

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