{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Costa CJ"],"funding":["CCR NIH HHS","Intramural NIH HHS","NIMHD NIH HHS","NCI NIH HHS","NIH HHS"],"pagination":["921"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11902232"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(5)"],"pubmed_abstract":["<h4>Background</h4>Chronic visceral hypersensitivity is associated with an overstressed pain response to noxious stimuli (hyperalgesia). Microbiota are active modulators of host biology and are implicated in the etiology of visceral hypersensitivity.<h4>Objectives</h4>we studied the association between the circulating mRNA transcriptome, the intensity of induced visceral pain (IVP), and variation in the oral microbiome among participants with and without baseline visceral hypersensitivity.<h4>Methods</h4>Transcriptomic profiles and microbial abundance were correlated with IVP intensity. Host mRNA and microbes associated with IVP were explored, linking variation in the microbiome to host RNA biology.<h4>Results</h4>259 OTUs were found to be associated with IVP through correlation to differential expression of 471 genes in molecular pathways related to inflammation and neural mechanisms, including Rho and PI3K/AKT pathways. The bacterial families Lachnospiraceae, Prevotellaceae, and Veillonellaceae showed the highest degree of association. Oral microbial profiles with reduced diversity were characteristic of participants with visceral hypersensitivity.<h4>Conclusions</h4>Our results suggest that the oral microbiome may be involved in systemic immune and inflammatory effects and play a role in nervous system and stem cell pathways. The interactions between visceral hypersensitivity, differentially expressed molecular pathways, and microbiota described here provide a framework for further work exploring the relationship between host and microbiome."],"journal":["Nutrients"],"pubmed_title":["Host Transcriptome and Microbial Variation in Relation to Visceral Hyperalgesia."],"pmcid":["PMC11902232"],"funding_grant_id":["1ZIANR000018-01-09; K22MD006143-01","K22 MD006143","HHSN261200800001E","ZIA NR000018","HHSN261200800001C"],"pubmed_authors":["Posada-Quintero H","Abey SK","Hoffman RK","Fourie NH","Sherwin LB","Rahim-Williams B","Henderson WA","Costa CJ","Prescott S","Joseph PV"],"additional_accession":[]},"is_claimable":false,"name":"Host Transcriptome and Microbial Variation in Relation to Visceral Hyperalgesia.","description":"<h4>Background</h4>Chronic visceral hypersensitivity is associated with an overstressed pain response to noxious stimuli (hyperalgesia). Microbiota are active modulators of host biology and are implicated in the etiology of visceral hypersensitivity.<h4>Objectives</h4>we studied the association between the circulating mRNA transcriptome, the intensity of induced visceral pain (IVP), and variation in the oral microbiome among participants with and without baseline visceral hypersensitivity.<h4>Methods</h4>Transcriptomic profiles and microbial abundance were correlated with IVP intensity. Host mRNA and microbes associated with IVP were explored, linking variation in the microbiome to host RNA biology.<h4>Results</h4>259 OTUs were found to be associated with IVP through correlation to differential expression of 471 genes in molecular pathways related to inflammation and neural mechanisms, including Rho and PI3K/AKT pathways. The bacterial families Lachnospiraceae, Prevotellaceae, and Veillonellaceae showed the highest degree of association. Oral microbial profiles with reduced diversity were characteristic of participants with visceral hypersensitivity.<h4>Conclusions</h4>Our results suggest that the oral microbiome may be involved in systemic immune and inflammatory effects and play a role in nervous system and stem cell pathways. The interactions between visceral hypersensitivity, differentially expressed molecular pathways, and microbiota described here provide a framework for further work exploring the relationship between host and microbiome.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2026-05-28T03:09:25.769Z","creation":"2025-04-03T23:57:20.882Z"},"accession":"S-EPMC11902232","cross_references":{"pubmed":["40077792"],"doi":["10.3390/nu17050921"]}}