RNA‑seq analysis of microglia from Fpr2 knockout and wild‑type mice following LPS‑induced acute inflammation

To investigate the molecular mechanisms by which formyl peptide receptor 2 (FPR2) regulates microglial activation and neuroinflammation in an LPS‑induced acute depression model, we performed RNA‑sequencing of microglia isolated from three groups of mice: wild‑type saline‑treated (WT‑Saline), wild‑type LPS‑treated (WT‑LPS), and Fpr2 knockout LPS‑treated (Fpr2‑/‑‑LPS). Transcriptomic profiling revealed that LPS challenge induced widespread changes in immune‑ and inflammation‑related pathways, including the NLR signaling pathway, cytokine‑cytokine receptor interaction, and chemokine signaling.

FPR2 deficiency partially reversed these LPS‑induced alterations, particularly suppressing the upregulation of genes involved in the NLRP3 inflammasome pathway (e.g., Nlrp3, Il1b, Csf1). These RNA‑seq data provide a global view of how FPR2 deletion reshapes the microglial transcriptome under inflammatory conditions and support the conclusion that FPR2 acts upstream of the CSF1/NLRP3 axis to mediate depressive‑like behaviors.