NPR-9 regulates the innate immune response in Caenorhabditis elegans by antagonizing the activity of AIB interneurons  

作　　者：Yonglin Yu Lingtong Zhi Qiuli Wu Lina Jing Dayong Wang 

机构地区：[1]Key Laboratory of Developmental Genes and Human Diseases in Ministry of Education,Medical School,Southeast University,Nanjing,210009,China

出　　处：《Cellular & Molecular Immunology》2018年第1期27-37,共11页中国免疫学杂志（英文版）

基　　金：Several nematode strains used in this study were provided by the CGC,which is funded by NIH Office of Research Infrastructure Program(P40 OD010440).

摘　　要：npr-9 encodes a homologue of the gastrin-releasing peptide receptor (GRPR) and is expressed in AIB interneurons. In this study, we investigated the role of NPR-9 in the neuronal control of innate immunity using the model system Caenorhabditis elegans. After exposure to Pseudomonas aeruginosa PA14, npr-9(tm1652) mutants showed resistance to infection, decreased PA14 colonization and increased expression of immunity-related genes. Nematodes overexpressing NPR-9 exhibited increased susceptibility to infection, increased PA14 colonization and reduced expression of immunity-related genes. In nematodes, ChR2-mediated AIB interneuron activation strengthened the innate immune response and decreased PA14 colonization. Overexpression of NPR-9 suppressed the innate immune response and increased PA14 colonization in nematodes with the activation of AIB interneurons mediated by ChR2 or by expressing pkc-1(gf) in AIB interneurons. We, therefore, hypothesize that NPR-9 regulates the innate immune response by antagonizing the activity of AIB interneurons. Furthermore, expression of GRPR, the human homologue of NPR-9, could largely mimic NPR-9 function by regulating innate immunity in nematodes. Our results provide insight into the pivotal role of interneurons in controlling innate immunity and the complex biological functions of GRPRs.

关 键 词：AIB interneuron Caenorhabditis elegans innate immunity neuronal basis NPR-9 

分 类 号：R57[医药卫生—消化系统]