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来自丝虫寄生虫塞氏栉鳞颚口线虫的具有高硫氧还蛋白还原酶 (TrxR) 酶活性的粗蛋白成分可抵抗脂多糖 (LPS) 诱导的巨噬细胞炎症。

Crude protein fraction with high thioredoxin reductase (TrxR) enzyme activity from filarial parasite Setaria cervi counters lipopolysaccharide (LPS)-induced inflammation in macrophages.

机构信息

Parasitology Laboratory, Department of Zoology, Siksha-Bhavana, Visva-Bharati University, Santiniketan, Bolpur, 731235, West Bengal, India.

Division of Molecular Medicine, Bose Institute, P-1/12, CIT Road Scheme VIIM, Kolkata, 700 054, West Bengal, India.

出版信息

Parasitol Res. 2022 May;121(5):1379-1388. doi: 10.1007/s00436-022-07495-7. Epub 2022 Mar 23.

DOI:10.1007/s00436-022-07495-7
PMID:35320838
Abstract

Host-parasite interaction has always been an area of interest to the parasite biologists. The complex immune interactions between the parasite and/or the parasite-derived products with the host immune cells determine the fate of the disease biology. Parasitic organisms are widely equipped with a vast array of protective machineries including antioxidant enzymes to withstand the hostile condition inside the host body. The reactive oxygen species (ROS) generated inside the host as a result of parasitic intervention can be endured by the parasite by their own tools to ensure their survival. One such antioxidant enzyme in the filarial parasite that plays a significant role in redox homeostasis, survivability and disease progression is the thioredoxin reductase (TrxR). Herein, we have projected a crude lysate of the bovine filarial parasite Setaria cervi enriched with high TrxR enzyme activity has the capacity to downregulate lipopolysaccharide (LPS)-induced inflammatory macrophages. TrxR-mediated inhibition of the TLR4-NF-κB axis resulting into downregulation of the pro-inflammatory cytokines with concomitant upregulation of the anti-inflammatory cytokines supports the filarial parasite to produce an anti-inflammatory milieu which ultimately promotes worm survivability inside the host and pathogenesis.

摘要

寄生虫与宿主的相互作用一直是寄生虫生物学家感兴趣的领域。寄生虫和/或寄生虫衍生产物与宿主免疫细胞之间复杂的免疫相互作用决定了疾病生物学的命运。寄生虫广泛拥有一系列包括抗氧化酶在内的保护机制,以抵御宿主体内的恶劣环境。寄生虫干预导致宿主内部产生的活性氧 (ROS) 可以被寄生虫自身的工具所耐受,以确保它们的生存。在丝虫寄生虫中,一种在氧化还原稳态、生存能力和疾病进展中起重要作用的抗氧化酶是硫氧还蛋白还原酶 (TrxR)。在这里,我们预测富含高 TrxR 酶活性的牛丝虫寄生虫粗提物能够下调脂多糖 (LPS) 诱导的炎症性巨噬细胞。TrxR 介导的 TLR4-NF-κB 轴抑制导致促炎细胞因子下调,同时抗炎细胞因子上调,支持丝虫寄生虫产生抗炎微环境,最终促进蠕虫在宿主内的生存能力和发病机制。

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本文引用的文献

1
Filarial thioredoxin reductase exerts anti-inflammatory effects upon lipopolysaccharide induced inflammation in macrophages.丝虫硫氧还蛋白还原酶对脂多糖诱导的巨噬细胞炎症具有抗炎作用。
Int J Biol Macromol. 2021 Dec 15;193(Pt B):1379-1390. doi: 10.1016/j.ijbiomac.2021.10.200. Epub 2021 Nov 10.