{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE285nnn/GSE285766/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":[" Genome binding/occupancy profiling by high throughput sequencing","Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE285766"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Single-cell multi-omic sequencing reveals cell-specific transcriptomic and chromatin accessibility profiles in gut microbiome metabolite butyrate-produced pain modulation","description":"Pain is a predominant symptom of temporomandibular joint (TMJ) disorders, presenting significant clinical challenges due to their complexity and limited treatment options. This study investigated the therapeutic potential of butyrate, a gut microbiome metabolite, in a complete Freund’s adjuvant (CFA)-induced mouse model of TMJ inflammatory pain. Butyrate administration significantly alleviated TMJ pain and restored butyrate levels in mouse feces, plasma, and the spinal trigeminal nucleus caudalis (Sp5C). Additionally, it reversed TMJ pain-induced reductions in acetylation within Sp5C neurons, a critical epigenetic mechanism linked to pain states. Utilizing single-nucleus RNA sequencing (snRNA-seq) and single-nucleus ATAC sequencing (snATAC-seq), we profiled transcriptional and chromatin accessibility changes at the single-cell level.","dates":{"publication":"2026/04/22"},"accession":"GSE285766","cross_references":{"GSM":["GSM8708535","GSM8708534","GSM8708545","GSM8708544","GSM8708543","GSM8708542","GSM8708541","GSM8708540","GSM8708539","GSM8708538","GSM8708537","GSM8708536"],"GPL":["24247"],"GSE":["285766"],"taxon":["Mus musculus"],"PMID":["[41997906]"]}}