PfHMGB2 protects yellow catfish (Pelteobagrus fulvidraco) from bacterial infection by promoting phagocytosis and proliferation of PBL
PfHMGB2 protects yellow catfish (Pelteobagrus fulvidraco) from bacterial infection by promoting phagocytosis and proliferation of PBL
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PfHMGB2 通过促进 PBL 的吞噬作用和增殖来保护黄颡鱼 (Pelteobagrus fulvidraco) 免受细菌感染
DOI：
10.1016/j.fsi.2019.08.007
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发表时间：
2019-10-01
影响因子：
4.7
通讯作者：
Ke，Fei
中科院分区：
文献类型：
--
作者：
Wang，Yun;Yang，Yanyan;Ke，Fei
HMGB2是高迁移性基团box家族的成员，在宿主免疫应答中起重要作用。然而，HMGB2的作用机制尚不清楚。本文克隆了黄颡鱼（Pelteobagrusfulvidraco）的同源基因，命名为PfHMGB2。推导出的PfHMGB2氨基酸序列具有典型的三方结构（两个DNA结合盒和一条酸尾），与mi预测的HMGB2具有90%的同源性。毛虫。PfHMGB2 mRNA广泛分布于健康鱼体的11个组织中，并在灭活的嗜水气单胞菌注射后在黄颡鱼的肝脏和头肾中被显著诱导。同样，脂多糖也可以诱导黄颡鱼外周血白细胞（PBL）中PfHMGB2mRNA的表达。从me中纯化重组PfHMGB2蛋白。coliBL21 (DE3):pET-28a/PfHMGB2，显示dna结合亲和力。rPfHMGB2提高了黄颡鱼PBL的吞噬和增殖活性，上调了促炎细胞因子TNFα的mRNA表达。这些结果表明，PfHMGB2可以通过激活PBL来保护黄颡鱼免受病原菌感染。
HMGB2, a member of the high mobility group box family, plays an important role in host immune responses. However, the mechanism of action of HMGB2 is not well understood. Herein, a homologue from yellow catfish (Pelteobagrusfulvidraco) was cloned and named PfHMGB2. The deduced amino acid sequence of PfHMGB2 possessed a typical tripartite structure (two DNA binding boxes and an acid tail) and shared 90% identity with the predicted HMGB2 fromI. punctatus. The mRNA of PfHMGB2 was widely distributed in all 11 tested tissues in healthy fish bodies and was significantly induced in the liver and head kidney when yellow catfish were injected with inactivatedAeromonashydrophila. Consistently,PfHMGB2mRNA could also be induced in yellow catfish peripheral blood leucocytes (PBL) by lipopolysaccharide. The recombinant PfHMGB2 protein was purified fromE. coliBL21 (DE3):pET-28a/PfHMGB2 and showed DNA-binding affinity. Moreover, rPfHMGB2 improved the phagocytosis and proliferation activity and upregulated the mRNA expression of the pro-inflammatory cytokine TNFα in yellow catfish PBL. These results indicated that PfHMGB2 could protect yellow catfish from pathogen infection by activating PBL.