Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Sciences, Shandong University, Qingdao, China.
State Key Laboratory of Microbial Technology, Shandong University, Qingdao, China.
EMBO Rep. 2023 May 4;24(5):e55903. doi: 10.15252/embr.202255903. Epub 2023 Mar 28.
In the arthropod gut, commensal microbiota maintain the immune deficiency (Imd)/Relish pathway for expression of antimicrobial peptides, whereas pathogenic bacteria induce dual oxidase 2 (Duox2) for production of extracellular microbicidal reactive oxygen species (ROS). The Imd/Relish pathway and the Duox2/ROS system are regarded as independent systems. Here, we report that these two systems are bridged by the tumor necrosis factor (TNF) ortholog PcEiger in the red swamp crayfish Procambarus clarkii. PcEiger expression is induced by commensal bacteria or the Imd/Relish pathway. PcEiger knockdown alters bacterial abundance and community composition due to variations in the oxidative status of the intestine. PcEiger induces Duox2 expression and ROS production by regulating the activity of the transcription factor Atf2. Moreover, PcEiger mediates regulation of the Duox2/ROS system by commensal bacteria and the Imd/Relish pathway. Our findings suggest that the Imd/Relish pathway regulates the Duox2/ROS system via PcEiger in P. clarkii, and they provide insights into the crosstalk between these two important mechanisms for arthropod intestinal immunity.
在节肢动物肠道中,共生微生物维持免疫缺陷 (Imd)/Relish 途径以表达抗菌肽,而致病性细菌诱导双氧化酶 2 (Duox2) 产生细胞外杀菌活性氧物质 (ROS)。Imd/Relish 途径和 Duox2/ROS 系统被认为是独立的系统。在这里,我们报告在克氏原螯虾 Procambarus clarkii 中,肿瘤坏死因子 (TNF) 直系同源物 PcEiger 将这两个系统联系起来。PcEiger 的表达受共生细菌或 Imd/Relish 途径诱导。PcEiger 敲低会由于肠道氧化状态的变化而改变细菌的丰度和群落组成。PcEiger 通过调节转录因子 Atf2 的活性诱导 Duox2 表达和 ROS 产生。此外,PcEiger 介导了共生细菌和 Imd/Relish 途径对 Duox2/ROS 系统的调节。我们的研究结果表明,在 P. clarkii 中,Imd/Relish 途径通过 PcEiger 调节 Duox2/ROS 系统,为这两个重要的节肢动物肠道免疫机制之间的串扰提供了新的见解。