Intact interleukin-10 receptor signaling protects from hippocampal damage elicited by experimental neurotropic virus infection of SJL mice

Differential interleukin-10 (IL-10) expression is suspected to contribute to strain specific differences in the course of Theiler's murine encephalomyelitis virus infection in mice. To determine the expression kinetics of IL-10 and related genes, RNA-based next generation sequencing (RNA-seq) was performed with brain cells obtained from infected SJL mice. Methods: 5-week old, female SJL mice were infected with the BeAn strain of TMEV and sacrificed 4, 7 or 14 days post infection (dpi). RNA was isolated from transversal sections of brain tissue at the level of the hippocampus. RNA-seq was performed on an Illumina HiSeq2500 system. Genes involved in Interleukin-10 (IL-10) signalling were analyzed and transcript levels were compared during the course of infection. Results: A significant upregulation of Interleukin-10 (Il10), Interleukin-10 receptor subunit α (ll10rα), Janus kinase 1 (Jak1) and signal transducer and activator of transcription 3 (Stat3) was detected 7 days post infection (dpi) compared to 4 dpi. Same genes showed a significant downregulation at 14 dpi compared to 7 dpi. Suppressor of cytokine signaling 3 (Socs3) was significantly downregulated at 14 dpi compared to 7 dpi. No differences were detected between transcript levels of interleukin-10 receptor subunit β (Il10rβ) and tyrosine kinase 2 (Tyk2). Conclusion: IL-10 pathway gene expression is transiently upregulated following TMEV-infection of SJL-mice. RNA-seq of brain tissue derived from TMEV-infected SJL mice. 3 different timepoints post infection with 5 animals per timepoint.