ArticleCell communication and signaling : CCS2025
tRF-His-GTG-1 promotes Salmonella survival through modulation of lipid metabolism and immune signaling.
Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- tRNA‑derived RNAs in hepatic diseases: From biological functions to clinical translation (Review).International journal of molecular medicine · 2026Review
- Longitudinal Immunophenotypic Changes in Refractory Lupus Nephritis After B-cell Depletion: A 25-year Case Study.In vivo (Athens, Greece)Article
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5 authors.
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Abstract
backgroundPatients with systemic lupus erythematosus (SLE) are highly susceptible to severe infections, with non-typhoidal Salmonella (NTS) often progressing to life-threatening bacteremia. However, the mechanisms underlying this heightened vulnerability remain unclear. Lipid droplets (LDs), key immunometabolic hubs, have been implicated in facilitating Salmonella survival within phagocytes. We identified the tRNA-derived small RNA (tsRNA) tRF-His-GTG-1 as upregulated in SLE and correlated with disease activity. This study investigates the signaling and functional roles of tRF-His-GTG-1 in LD formation and Salmonella persistence in SLE.
methodsLDs and tRF-His-GTG-1 expression were analyzed in peripheral blood mononuclear cells (PBMCs) from SLE patients with or without NTS bacteremia and from controls. Bacterial survival, tsRNA function, and signaling pathways were assessed using immunofluorescence, qRT-PCR, colony-forming unit assays, and pharmacological or genetic inhibition.
resultsLDs were elevated in SLE PBMCs and further increased by NTS infection, correlating with enhanced bacterial survival. SLE immune complexes (ICs) and IC-primed platelet-derived extracellular vesicles (pEVs) induced LD formation via FcγRIIA-mediated uptake and Toll-like receptor (TLR) 7/8 activation. Both SLE ICs and NTS infection upregulated tRF-His-GTG-1. Mechanistically, tRF-His-GTG-1 directly bound to TLR7/8, activating ERK/p38 signaling to induce PPARδ expression and LD biogenesis. Concurrently, tRF-His-GTG-1 promoted ERK/p38 phosphorylation and IL-10 production. Inhibition of tRF-His-GTG-1 suppressed both LD- and IL-10-dependent pathways, thereby reducing Salmonella survival.
conclusionstRF-His-GTG-1 enhances Salmonella persistence through a TLR7/8-ERK/p38-PPARδ/IL-10 signaling axis. These findings identify a tsRNA-mediated immunometabolic mechanism linking SLE with bacterial susceptibility and highlight tRF-His-GTG-1 as a potential therapeutic target to improve antibacterial immunity in high-risk patients.
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