{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gumas J"],"funding":["National Institute of Allergy and Infectious Diseases","American Cancer Society","NIAID NIH HHS","NHLBI NIH HHS","National Institutes of Health","National Heart Lung and Blood Institute","National Institute of General Medical Sciences","NIGMS NIH HHS"],"pagination":["102156"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10933579"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["35(1)"],"pubmed_abstract":["<i>Mycobacterium tuberculosis</i> (Mtb) infection is among the world's deadliest infectious diseases. Developing effective treatments and biomarkers for tuberculosis requires a deeper understanding of its pathobiology and host responses. Here, we report a comprehensive characterization of circulating short non-coding RNAs (sncRNAs) in plasma samples from Mtb-infected patients. We achieved this by pre-treating plasma RNAs with T4 polynucleotide kinase to convert all RNA ends to those compatible with sncRNA sequencing. We discovered a global and drastic upregulation of plasma sncRNAs in Mtb-infected patients, with tRNA-derived sncRNAs representing the most dramatically elevated class. Most of these tRNA-derived sncRNAs originated from a limited subset of tRNAs, specifically from three tRNA isoacceptors, and exhibited skewed patterns to 5'-derived fragments, such as 5' halves, 5' tRNA fragments (tRFs), and internal tRFs (i-tRFs) from the 5' regions. Further, Mtb-infected patients displayed markedly upregulated and distinct profiles of both rRNA- and mRNA-derived sncRNAs. Some of these sncRNAs, which are abundant and specific to Mtb-infected patients, robustly activated human macrophages via Toll-like receptor 7 and induced cytokine production. This drastic accumulation of circulating, immunostimulatory sncRNAs in the plasma of Mtb-infected patients offers insights into the sncRNA-driven aspects of host immune response against infectious diseases and suggests a pool of potential therapeutic targets and biomarkers."],"journal":["Molecular therapy. Nucleic acids"],"pubmed_title":["Immunostimulatory short non-coding RNAs in the circulation of patients with tuberculosis infection."],"pmcid":["PMC10933579"],"funding_grant_id":["R21 AI171366","R01 HL150560","AI168975","R21 AI168975","HL150560","GM106047","R01 GM106047","R21 AI151641","RSG-17-059-01-RMC","AI151641","AI171366"],"pubmed_authors":["Gumas J","Kirino Y","Shigematsu M","Kawamura T"],"additional_accession":[]},"is_claimable":false,"name":"Immunostimulatory short non-coding RNAs in the circulation of patients with tuberculosis infection.","description":"<i>Mycobacterium tuberculosis</i> (Mtb) infection is among the world's deadliest infectious diseases. Developing effective treatments and biomarkers for tuberculosis requires a deeper understanding of its pathobiology and host responses. Here, we report a comprehensive characterization of circulating short non-coding RNAs (sncRNAs) in plasma samples from Mtb-infected patients. We achieved this by pre-treating plasma RNAs with T4 polynucleotide kinase to convert all RNA ends to those compatible with sncRNA sequencing. We discovered a global and drastic upregulation of plasma sncRNAs in Mtb-infected patients, with tRNA-derived sncRNAs representing the most dramatically elevated class. Most of these tRNA-derived sncRNAs originated from a limited subset of tRNAs, specifically from three tRNA isoacceptors, and exhibited skewed patterns to 5'-derived fragments, such as 5' halves, 5' tRNA fragments (tRFs), and internal tRFs (i-tRFs) from the 5' regions. Further, Mtb-infected patients displayed markedly upregulated and distinct profiles of both rRNA- and mRNA-derived sncRNAs. Some of these sncRNAs, which are abundant and specific to Mtb-infected patients, robustly activated human macrophages via Toll-like receptor 7 and induced cytokine production. This drastic accumulation of circulating, immunostimulatory sncRNAs in the plasma of Mtb-infected patients offers insights into the sncRNA-driven aspects of host immune response against infectious diseases and suggests a pool of potential therapeutic targets and biomarkers.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Mar","modification":"2026-06-02T19:21:06.646Z","creation":"2025-02-19T04:41:51.589Z"},"accession":"S-EPMC10933579","cross_references":{"pubmed":["38481936"],"doi":["10.1016/j.omtn.2024.102156"]}}