表面分子在利什曼病宿主反应中的作用:以脂质介质为重点

A. Fattahi bafghi, F. Zare, Mostafa Gholamrezaei, Mahin Ghafourzadeh
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引用次数: 0

摘要

利什曼病是一种被忽视的疾病,影响着全世界1200多万人。雌性吸血昆虫(如白蛉)接种寄生虫后,中性粒细胞迅速浸润并吞噬利什曼原虫寄生虫。巨噬细胞是第二免疫细胞。它们具有多种模式识别受体,可响应不同的表面分子,如脂磷酸聚糖、糖蛋白63 (GP63)、PPG、GIPL、CP和SAP。研究发现,利什曼原虫GP63可切割感染巨噬细胞的几个靶点,包括肉豆荚酰化的富丙氨酸C激酶底物、p130CAS、PEST、NF-B和AP-1。经表面分子活化后,花生四烯酸的脂质代谢产物,包括白三烯和前列腺素,是利什曼病的重要介质。这些脂质代谢产物可以被不同的酶代谢,包括环加氧酶和脂加氧酶。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Role of Surface Molecules in Host Responses of Leishmaniasis: Focus on Lipid Mediators
Leishmaniasis is a neglected disease that affects more than 12 million people worldwide. After parasite inoculum by female blood-sucking insects, e.g. Phlebotomus, neutrophils quickly infiltrate and phagocytes Leishmania parasites. Macrophages are the second immune cells. They possess several pattern recognition receptors that respond to different surface molecules such as Lipophosphoglycan, glycoprotein 63 (GP63), PPG, GIPL, CP, and SAP. It was found that Leishmania GP63 cleaves several targets of infected macrophages, including the myristoylated alanine-rich C kinase substrate, p130CAS, PEST, NF-B, and AP-1. After activation of surface molecules, lipid metabolites of arachidonic acid, including leukotrienes and prostaglandins, are important mediators in Leishmaniasis. These lipid metabolites can be metabolized by different enzymes, including the cyclooxygenase and lipoxygenase.
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