Nucleotide-Binding Oligomerization Domain 1 (NOD1) Positively Regulates microglia-driven inflammatory response during Pseudorabies Virus Infection
The main cause of viral encephalitis is that the virus invades the central nervous system (CNS) and causes neuroinflammation, which poses a serious threat to the world's public health. Microgliaare CNS-resident macrophages that playanimportantroleinneuroinflammation and thus often identified as target of choice for the prevention or treatment of viral encephalitis. Nucleotide-binding oligomerization domain 1 (NOD1) is a type of pattern recognition receptor and has been associated with many inflammatory diseases in humans. Here, we used pseudorabiesvirus (PRV) as a model to examine the regulation of microglia responses during viral encephalitis and discuss whether NOD1 suppressed neuroinflammation by regulating microglial activation. Cellular experiments indicated that microglia activation accompanying by cell migration, characteristic morphological changes, phagocytosis, inflammatory cytokine production and antigen presentation. We then investigated the effect of NOD1 on the PRV-induced microglia activation. Theresultsinvitro and in vivoshowedthat PRV infection upregulated the mRNA and protein expression of NOD1. Inhibition or overexpression of NOD1 can reduce or enhance the activation JNK and NF-?B signal pathway to regulate the microglia activation and inflammatory response induced by PRV. Overall design: Comparative gene expression profiling analysins of RNA-seq data for BV2 cells with or without PRV