Abstract: The study aimed to explore the mechanism of brain tissue injury caused by Enterococcus faecalis, a brain injury model from the mice infected with E. faecalis was constructed. Pathological observation and transcriptomic difference analysis for different period of infection were conducted. In this experiment, a strain of E. meningitidis was selected. Mice were used as infected animals. After being infected with E. faecalis, the brain tissues of mice were collected in time periods:at 2, 4, 6, 12, 24, 36, 60 and 72 h, separately. Then, the degree of brain tissue damage were observed. Three time points:early stage, obvious stage and prognosis stage, were selected to analyze differentially expressed genes by transcriptomic sequencing, and fluorescent quantitative PCR was used to verify the transcriptomic data. After 12 h, lesions occurred in the brain tissues of the mice infected. Histopathological observation showed that the meninges presented and brain tissue blood vessels were congested successively in the mouse brain tissue. The perivascular space was widened, and the brain tissue presented grid gap due to edema. Microthrombosis and inflammatory cell occurred. For transcriptomic differential gene analysis, the GO enrichment results showed that the main enrichment was the response to interferon-β, the response of cells to interferon-β, the defense response to other organisms, the response to interferon-γ, the response to bacteria, response, extrinsic apoptosis signaling pathway, regulation of extrinsic apoptosis signaling pathway, neuronal apoptosis process, endothelial cell migration and other biological processes. KEGG enrichment results showed that differential signaling pathways were mainly enriched relative signal paths related to brain tissue damage:peroxisome, NOD-like receptor signaling pathway, oxidative phosphorylation, calcium metabolism signaling pathway, PI3K-Akt signaling pathway, Wnt signaling pathway, MAPK signaling pathway, GnRH secretion, VEGF signaling pathway, tight junction and some other related pathways. After the infection of mice, E. faecalis affected the brain tissue peroxisome, NOD-like receptor signaling pathway, oxidative phosphorylation, calcium metabolism signaling pathway, PI3K-Akt signaling pathway and other pathways. These are related to protein phosphorylation, the occurrence of inflammation and the change of the permeability of the blood-brain barrier. The study conclusion provides a research direction and theoretical basis for further research on the mechanism of brain tissue damage caused by E. faecalis.

Key words: Enterococcus faecalis, mice, meningitis, pathology, differential genes