期刊
SCIENTIFIC REPORTS
卷 11, 期 1, 页码 -出版社
NATURE PORTFOLIO
DOI: 10.1038/s41598-021-86125-1
关键词
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资金
- Australian Government RTPS Scholarship
- FCT, Portugal [UIDB/04046/2020, UIDP/04046/2020]
- BioSys PhD programme from FCT (Portugal) [PD65-2012, SFRH/PD/BD/142854/2018]
- Science Foundation Ireland (SFI) [17/RP/5368]
- Science Foundation Ireland (SFI) [17/RP/5368] Funding Source: Science Foundation Ireland (SFI)
The parasite Fasciola hepatica regulates host innate immune responses by releasing miRNA, especially fhe-miR-125b, which mimics host miRNA to negatively regulate the production of inflammatory cytokines. This manipulation of the miRNA machinery controlling innate cell function is a fundamental mechanism by which worm parasites disarm the early immune responses of their host to ensure successful infection.
Fasciola hepatica, a global worm parasite of humans and their livestock, regulates host innate immune responses within hours of infection. Host macrophages, essential to the first-line defence mechanisms, are quickly restricted in their ability to initiate a classic protective pro-inflammatory immune response. We found that macrophages from infected animals are enriched with parasite-derived micro(mi)RNAs. The most abundant of these miRNAs, fhe-miR-125b, is released by the parasite via exosomes and is homologous to a mammalian miRNA, hsa-miR-125b, that is known to regulate the activation of pro-inflammatory M1 macrophages. We show that the parasite fhe-miR-125b loads onto the mammalian Argonaut protein (Ago-2) within macrophages during infection and, therefore, propose that it mimics host miR-125b to negatively regulate the production of inflammatory cytokines. The hijacking of the miRNA machinery controlling innate cell function could be a fundamental mechanism by which worm parasites disarm the early immune responses of their host to ensure successful infection.
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