Effect of depletion of NLRC3 on glycolytic genes of macrophage with LPS treatment

The impaired aerobic glycolysis of monocyte/macrophage are the main features in sepsis that encountered immunosuppression. NLRC3, an inhibitory sensor, can diminish the Toll-like receptor 4 pathways of macrophages which is associated with sepsis-induced immunosuppression, but whether NLRC3 plays key role in regulating the immunosuppression of macrophage via interfering glycolysis still unclear. The aim of this study was to characterize the transcriptome alterations by which NLRC3 loss, and further investigate the role of the glycolysis in the macrophage with the development of sepsis. Bone marrow-derived macrophages (BMDMs) was isolated from the femurs and tibias of the NLRC3 WT (LysM-Cre-NLRC3fl/fl) and NLRC3ΔMac (LysM-Cre+ NLRC3fl/fl) mice and then was treated with or without LPS for 12 hours, and the macrophages mRNA profiles of five-weeks-old NLRC3 WT mice (WT macrophages) and of five-weeks-old NLRC3ΔMac mice (NLRC3-/- macrophages) were generated by deep sequencing, in triplicate, using Illumina 6000. Bone marrow-derived macrophages (BMDMs) was isolated from the femurs and tibias of the NLRC3 WT (LysM-Cre-NLRC3fl/fl) and NLRC3ΔMac (LysM-Cre+ NLRC3fl/fl) mice and then treated with or without LPS for 12 hours.