
Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16
Published: April 14, 2025
Background Recent studies have highlighted the importance of cross-talk along gut-brain axis in regulating inflammatory nociception, responses, and immune homeostasis. The gut microbiota, particularly its bacterial composition, plays a crucial role development function system. Moreover, metabolites produced by microbiota can significantly impact both systemic responses central nervous system (CNS) immunity. Sodium butyrate is key metabolite and, as histone deacetylase inhibitor, enhance anti-tumor immunity cytotoxic CD8 + T cells. However, it remains unclear whether sodium treatment efficacy PD-1 blockade glioma therapy. In this research, effect underlying mechanism combination anti-mouse mAb on has been investigated. Methods RNA-seq assay cell biomedical databases, including ONCOMINE, GEPIA TCGA were incorporated. Subsequently, inhibitory cells related mechanisms assessed through Counting Kit-8 (CCK-8), Flow Cytometry, Western blot (WB), reverse transcription-quantitative polymerase chain reaction (RT-qPCR), other vitro experiments. , an orthotopic mouse model was established. MRI imaging, Immunohistochemistry, Immune flow cytometry used to investigate therapeutic effects combined inhibitor glioma-bearing mice. Results We discovered that deacetylation-associated gene expression increased patients affects patient survival time. we found promoted apoptosis, disrupted cycle, inhibited tumor growth. Additionally, may upregulate PD-L1 modulating PI3K/AKT pathway. experimental results demonstrated therapy reduced volume prolonged murine model. led increase proportion probiotic bacteria resulting elevated levels antitumor decrease affect function.
Language: Английский