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Tearing Down the Wall: emu-miR-745-3p in Echinococcus multilocularis Exosomes Attenuates Host Liver Fibrosis to
Ning Yang1,2, Hongbin Zhang1, Bowen Shi1
1State Key Laboratory of Pathogenesis, Prevention, and Treatment of Central Asian High Incidence Diseases, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, PR China.
Background:
Alveolar echinococcosis (AE), caused by Echinococcus multilocularis (E. multilocularis), exhibits tumor-like, invasive growth in the liver. Unlike cystic echinococcosis, AE lesions are bordered by loose fibrosis, not a dense capsule. How the parasite weakens this host fibrotic response remians unknown.
Methods:
We identified functional miRNAs in parasite-derived exosomes via small RNA sequencing and multi-step screening, validated them using bioinformatics, luciferase assays, and in vitro studies in hepatic stellate cell studies (HSCs) and inhibited the target in vivo with AAV6-delivered TuD RNA in mice.
Results:
Exosomal emu-miR-745-3p from E. multilocularis targets DPP4 in HSCs, suppressing their activation and reducing fibrotic markers (α-SMA, COL1A1, TIMP1). In vivo inhibition of this miRNA increased perilesional fibrosis and capsule thickness, and decreased parasite burden.
Conclusions:
E. multilocularis employs exosomal emu-miR-745-3p to attenuate host fibrotic encapsulation, facilitating invasive growth. The emu-miR-745-3p/DPP4 axis is a critical determinant of AE pathology and a potential target for novel anti-fibrotic therapeutics.
