ArticleVeterinary research2025
GHSR gene knockout alleviates the liver pathological response in Echinococcus granulosus infection by reducing parasite survival.
Article in Veterinary research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed.
- PLGA - encapsulated harmine derivative H-2-168: A promising therapeutic agent for mitigating liver damage in hepatic hydatid disease.PLoS neglected tropical diseases · 2026Article
- GHSR and TLR4 collectively promote hepatic inflammation and aberrant repair in alveolar echinococcosis.Frontiers in immunology · 2026Article
- Affective-cognitive circuits in postoperative appetite reduction: an adaptive neuroimmune response to surgical stress.Frontiers in neuroscience · 2025Review
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Authors and funding
9 authors.
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Abstract
Cystic echinococcosis (CE) is a parasitic disease caused by the larval stage of Echinococcus granulosus, and the immunosuppressive microenvironment exacerbates disease progression. Ghrelin, a peptide hormone, plays a role in modulating immune inflammation and may influence the progression of E. granulosus infection through its receptor, GHSR (growth hormone secretagogue receptor). However, whether GHSR downregulation can inhibit E. granulosus infection remains unclear. In this study, we extracted liver tissues from E. granulosus-infected mice and those treated with the GHSR antagonist [D-Lys3]-GHRP-6. Proteomic analysis revealed 341 differentially expressed proteins, of which 185 were upregulated and 156 were downregulated. Metabolomic sequencing revealed 101 differentially expressed metabolites, including 62 upregulated and 39 downregulated metabolites. KEGG pathway enrichment analysis of both proteomic and metabolomic data revealed seven key signalling pathways, 11 key proteins, and 26 key metabolites that interact through metabolic and organic system networks. Next, we examined the disease progression of E. granulosus infection in GHSR-knockout mice. Compared with the E. granulosus (Eg) group, the GHSR-KO group presented a significant reduction in the number of liver infection foci. The serum and liver ghrelin levels were significantly greater in the E. granulosus group than in the control group, along with increased secretion of proinflammatory cytokines (IL-2 and IFN-γ) and decreased secretion of anti-inflammatory cytokines (IL-4 and IL-10). In contrast, the GHSR-KO group presented significantly lower ghrelin levels in both the serum and liver, with reduced proinflammatory cytokine secretion and increased anti-inflammatory cytokine secretion, similar to those of the control group. Furthermore, ghrelin and inflammation-related factors, including MyD88, NF-κB p65, iNOS, and Arg-1, exhibited coordinated expression changes in liver lesions and surrounding areas. These findings suggest that GHSR gene knockout can ameliorate the progression of liver E. granulosus infection and associated liver inflammation.
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Registered trials
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