Peripheral Immune Cell Infiltration in the Hippocampus of Sepsis Mice

Peripheral immune cell infiltration plays a key role in the excessive intracranial inflammatory response during sepsis, contributing to cognitive dysfunction and increased mortality. This study aims to elucidate the immune inflammatory status of hippocampal tissue in septic mice, providing potential targets for treatment and prevention. Male C57BL/6J mice underwent cecal ligation and puncture (CLP) or sham surgery. Twenty-four hours post-surgery, hippocampal tissues were harvested for transcriptome sequencing and immunofluorescence analysis. Immune cell infiltration was assessed using the xCell package, and structural changes in brain microvessels were evaluated by transmission electron microscopy. Flow cytometry and immunofluorescence confirmed immune cell presence in the hippocampus. Hub genes related to immune responses were identified using protein-protein interaction networks, weighted gene co-expression network analysis, and enrichment analysis of immune-related biological processes. In CLP mice, microvessel endothelial cells were separated, with swelling and damage to tight junctions. Significant infiltration of myeloid immune cells, including dendritic cells, monocytes and neutrophils, was observed in the hippocampus. Seven immune-related hub genes (Fcer1g, Fcgr2b, Fcgr3, Icam1, Itgb2, Ptprc and Slc11a1) play a pivotal role in mediating immune responses. Fcer1g, Fcgr2b and Slc11a1 were positively correlated with monocytes and neutrophils, suggesting their involvement in the recruitment of immune cells to the brain. This study enhances our understanding of peripheral immune cell infiltration in sepsis and provides novel insights into potential therapeutic targets for sepsis-associated encephalopathy.