Evidence map›Paper›PMID 40452071›Full record

ArticleParasites & vectors2025

miRNA let-7-5p present in the extracellular vesicles of Trichinella spiralis newborn larvae inhibits the function of M1-type RAW264.7 macrophages by targeting C/EBPδ.

Yi Liu, Yu Chun Cai, Jia Xu Chen, Shao Hong Chen, Ying Fang Yu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Parasites & vectors, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Trichinellosis: A zoonosis that still requires vigilance.PLoS neglected tropical diseases · 2026
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Yi LiuNational Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention (Chinese Center for Tropical Diseases Research); National Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases; National Health Commission Key Laboratory On Parasite and Vector Biology, WHO Collaborating Centre for Tropical Diseases, National Center for International Research on Tropical Diseases, Ministry of Science and Technology, Shanghai, 200025, China.
Yu Chun CaiNational Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention (Chinese Center for Tropical Diseases Research); National Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases; National Health Commission Key Laboratory On Parasite and Vector Biology, WHO Collaborating Centre for Tropical Diseases, National Center for International Research on Tropical Diseases, Ministry of Science and Technology, Shanghai, 200025, China.
Jia Xu ChenNational Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention (Chinese Center for Tropical Diseases Research); National Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases; National Health Commission Key Laboratory On Parasite and Vector Biology, WHO Collaborating Centre for Tropical Diseases, National Center for International Research on Tropical Diseases, Ministry of Science and Technology, Shanghai, 200025, China. chenjx@nipd.chinacdc.cn.
Shao Hong ChenNational Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention (Chinese Center for Tropical Diseases Research); National Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases; National Health Commission Key Laboratory On Parasite and Vector Biology, WHO Collaborating Centre for Tropical Diseases, National Center for International Research on Tropical Diseases, Ministry of Science and Technology, Shanghai, 200025, China.
Ying Fang YuNational Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention (Chinese Center for Tropical Diseases Research); National Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases; National Health Commission Key Laboratory On Parasite and Vector Biology, WHO Collaborating Centre for Tropical Diseases, National Center for International Research on Tropical Diseases, Ministry of Science and Technology, Shanghai, 200025, China.

Funding

National Key Research and Development Program of China 2021YFC2300800National Science and Technology Infrastructure Platform National Parasite Resource Bank Project NPRC 2019 194 30
6 · The paper itself

Abstract

backgroundTrichinella spiralis, in its newborn larva (NBL) stage, invades the host bloodstream and disseminates throughout the body. Concurrently, M1 macrophages undergo transformation into M2 macrophages. In our previous studies, we demonstrated that extracellular vesicles secreted by NBL (NBL-EVs) significantly express the microRNA (miRNA) cel-let-7-5p. In this study, we investigated the immunomodulatory effects and mechanisms of action of EVs derived from T. spiralis NBL and the influence of their key miRNA, cel-let-7-5p, on M1 macrophages.

methodsThis study investigates the impact of T. spiralis NBL-EVs and cel-let-7-5p on RAW264.7 macrophages through in vitro co-culture, followed by a dual luciferase assay to confirm C/EBPδ as the target of cel-let-7-5p. M1-polarized RAW264.7 cells were subsequently transfected with various agents, including NBL-EVs, cel-let-7-5p mimic, C/EBPδ small interfering RNA (siRNA), and so forth. The cell functions, surface molecule expression, transcription, and cytokine release were analyzed using flow cytometry, reverse transcription polymerase chain reaction (RT-PCR), western blot, and enzyme-linked immunosorbent assay (ELISA) to elucidate the regulatory mechanisms of NBL-EVs and cel-let-7-5p on macrophage polarization.

resultsResults show that cel-let-7-5p transported by T. spiralis NBL-EVs inhibited the functional activity of M1 RAW264.7 macrophages by targeting C/EBPδ. This inhibition was validated by reduced CD86 and increased CD206 expression, along with decreased nitric oxide (NO) synthesis and downregulation of the M1 marker genes interleukin-12 (IL-12) and inducible nitric oxide synthase (iNOS). In contrast, the messenger RNA (mRNA) levels of IL-10 and arginase-1 (Arg1), which are M2 characteristic genes, were significantly enhanced. However, the release of M1 pro-inflammatory cytokines, such as IL-6, tumor necrosis factor-alpha (TNF-α), and IL-1β, was decreased proportionally. Notably, introducing a cel-let-7-5p inhibitor effectively reversed the suppressive effect of NBL-EVs on M1 macrophage function and partially mitigated their transition to the M2 phenotype, notably impacting Arg1 gene expression. However, no significant changes were observed in CD206 protein expression or IL-10 mRNA levels.

conclusionsThe findings of this study reveal that cel-let-7-5p in T. spiralis NBL-EVs can inhibit the function of M1-type RAW264.7 macrophages by targeting C/EBPδ.

Indexed as

CCAAT-Enhancer-Binding Protein-deltaExtracellular VesiclesMacrophagesMicroRNAsTrichinella spiralisAnimalsCytokinesLarvaMiceRAW 264.7 CellsCCAAT-Enhancer-Binding Protein-deltaCytokinesMicroRNAsmirnlet7 microRNA, mouseC/EBPδExtracellular vesicleslet-7-5pMacrophagesNewborn larvaeTrichinella spiralis

Identifiers

PMID40452071
PMCPMC12126876

What Socratic holds

Textmetadata
LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.