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A novel C-type lectin LvCTL 4.2 has antibacterial activity but facilitates WSSV infection in shrimp (L. vannamei)
Developmental & Comparative Immunology ( IF 2.7 ) Pub Date : 2021-08-20 , DOI: 10.1016/j.dci.2021.104239
Yu-Hsun Huang, Ramya Kumar, Chun-Hung Liu, Shih-Shun Lin, Han-Ching Wang

Glycan-binding protein C-type lectin (CTL), one of the pattern recognition receptors (PRRs), binds to carbohydrates on the surface of pathogens and elicits antimicrobial responses in shrimp innate immunity. The objective was to identify and characterize a novel C-type lectin LvCTL 4.2 in Litopenaeus vannamei. The LvCTL 4.2 protein consisted of a signal peptide at the N terminal and a carbohydrate-recognition domain (CRD) with a mutated mannose-binding (Glu-Pro-Ala; EPA) motif at the C terminal, and thereby has a putative secreted mannose-binding C-type lectin architecture. LvCTL 4.2 was highly expressed in nervous tissue and stomach. Infection with white spot syndrome virus (WSSV) induced expression of LvCTL 4.2 in shrimp stomach at 12 h post infection. Conversely, there was no obvious upregulation in expression of LvCTL 4.2 in stomach or hepatopancreas of shrimp with AHPND (acute hepatopancreas necrosis disease). Pathogen binding assays confirmed recombinant LvCTL 4.2 protein (rLvCTL 4.2) had significant binding ability with the WSSV virion, Gram-negative, and Gram-positive bacteria. Moreover, rLvCTL 4.2 had strong growth inhibition of Vibrio parahaemolyticus. Silencing LvCTL 4.2 suppressed WSSV replication, whereas pretreatment of WSSV with rLvCTL 4.2 facilitated viral replication in vivo. In conclusion, LvCTL 4.2 acted as a PRR that inhibited AHPND-causing bacteria, but facilitated WSSV pathogenesis.



中文翻译:

一种新型 C 型凝集素 LvCTL 4.2 具有抗菌活性,但促进虾(南美白对虾)的 WSSV 感染

聚糖结合蛋白 C 型凝集素 (CTL) 是模式识别受体 (PRR) 的一种,与病原体表面的碳水化合物结合并在虾先天免疫中引发抗菌反应。目的是在南美白对虾中鉴定和表征一种新型 C 型凝集素 LvCTL 4.2. LvCTL 4.2 蛋白由 N 末端的信号肽和 C 末端具有突变的甘露糖结合 (Glu-Pro-Ala; EPA) 基序的碳水化合物识别域 (CRD) 组成,因此具有推定的分泌甘露糖-结合C型凝集素结构。LvCTL 4.2在神经组织和胃中高表达。白斑综合征病毒 (WSSV) 感染后 12 小时在虾胃中诱导 LvCTL 4.2 的表达。相反,AHPND(急性肝胰腺坏死病)虾的胃或肝胰腺中LvCTL 4.2的表达没有明显上调。病原体结合测定证实重组 LvCTL 4.2 蛋白 (rLvCTL 4.2) 与 WSSV 病毒粒子、革兰氏阴性和革兰氏阳性细菌具有显着的结合能力。此外,rLvCTL 4.2 对副溶血性弧菌。沉默 LvCTL 4.2 抑制了 WSSV 复制,而用 rLvCTL 4.2 预处理 WSSV 促进了体内病毒复制。总之,LvCTL 4.2 作为 PRR 可抑制引起 AHPND 的细菌,但促进 WSSV 发病机制。

更新日期:2021-09-03
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