节点1
先天免疫系统
炎症
生物
小RNA
下调和上调
免疫系统
脂多糖
信号转导
NF-κB
促炎细胞因子
免疫学
细胞生物学
细胞因子
癌症研究
节点2
遗传学
基因
作者
Qing Chu,Dekun Bi,Weiwei Zheng,Tianjun Xu
标识
DOI:10.1007/s11427-020-1777-y
摘要
Inflammation is a self-protection mechanism that can be triggered when innate immune cells detect infection. Eradication of pathogen infection requires appropriate immune and inflammatory responses, but excessive inflammatory responses can cause uncontrolled inflammation, autoimmune diseases, or pathogen dissemination. Mounting evidence has shown that microRNAs (miRNAs) in mammals act as important and versatile regulators of innate immunity and inflammation. However, miRNA-mediated regulation networks are largely unknown in inflammatory responses in lower vertebrates. Here miR-144 and miR-217 are identified as negative regulators in teleost inflammatory responses. We find that Vibrio harveyi and lipopolysaccharide (LPS) treatment significantly upregulate the expression of fish miR-144 and miR-217. Upregulated miR-144 and miR-217 suppress LPS-induced inflammatory cytokine expression by targeting nucleotide-binding oligomerization domain-containing protein 1 (NOD1), thereby avoiding excessive inflammatory responses. In addition, miR-144 and miR-217 regulate inflammatory responses through NOD1-induced nuclear factor kappa (NF-kB) signaling pathways. These findings demonstrate that miR-144 and miR-217 play regulatory roles in inflammatory responses by modulating the NOD1-induced NF-κB signaling pathway.
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