ArticleParasites & vectors2026
Therapeutic effects of IL-33/ST-2 pathway inhibition combined with albendazole on hepatic fibrosis and immune regulation in alveolar echinococcosis: in vivo and in vitro evidence.
Article in Parasites & vectors, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThis study aimed to examine the role of the interleukin-33 (IL-33)/suppression of tumorigenicity 2 (ST-2) signaling pathway in hepatic fibrogenesis within the microenvironment of alveolar echinococcosis (AE). The therapeutic efficacy and immunomodulatory effects of concurrent IL-33/ST-2 pathway inhibition and albendazole (ABZ) treatment were also evaluated.
methodsProtein expression levels of IL-33 and ST-2 in liver were examined in a murine model of AE using immunohistochemistry. Flow cytometry was used to detect the expression of IL-33 and ST-2 on eosinophils in the blood, liver, and spleen, respectively. Phagocytosis assays, migration assays, and western blot analysis were performed to investigate the effects of IL-33 and ST-2 on eosinophils and hepatic stellate cells, so as to evaluate their roles in hepatic fibrosis and eosinophil activity. Following targeted suppression of the IL-33/ST-2 signaling pathway in combination with ABZ administration, hepatic fibrosis in liver and therapeutic outcomes were assessed through Masson staining, western blot analysis, and liver index measurements. Immune function was assessed via spleen index evaluation and enzyme-linked immunosorbent assay in blood, while hepatic function was assessed by measuring serum alanine aminotransferase and aspartate aminotransferase levels.
resultsThe AE model demonstrated elevated expression of IL-33 and ST-2 in hepatic tissues. In vitro analyses indicated that IL-33 and ST-2 promoted profibrotic phenotypes, including upregulation of α-smooth muscle actin (α-SMA), in hepatic stellate cells, supporting their role in fibrosis development, and modulated eosinophil activity. Inhibition of IL-33/ST-2 expression, followed by ABZ administration, enhanced therapeutic efficacy, improved liver function parameters, and modulated immune responses in AE mice. Combined therapy led to superior outcomes compared with monotherapy, with evidence of reduced hepatic injury and restored immunological homeostasis.
conclusionsThe IL-33/ST-2 signaling pathway contributes to the pathogenesis of hepatic fibrosis and immunological dysregulation in AE by influencing eosinophil function. Combined intervention targeting this pathway and albendazole administration confers enhanced therapeutic efficacy for AE, encompassing antifibrotic action, liver function recovery, and immune modulation.
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