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This research investigates the role of interleukin-33 in fibrosis development around hepatic alveolar echinococcosis lesions.

February 2, 2026Open Access

Exploring the Potential Role of Interleukin-33 in Inducing Eosinophil-Mediated Fibrosis in Hepatic Alveolar Echinococcosis

Key Points

This research investigates the role of interleukin-33 in fibrosis development around hepatic alveolar echinococcosis lesions.
Compared IL-33/ST-2 levels in patients with HAE and healthy controls using ELISA, western blot, and immunohistochemistry.
Performed co-localization analysis for IL-33/ST-2 and eosinophils using immunofluorescence.
Evaluated fibrosis in AE lesions using Masson's trichrome staining.
Conducted cellular assays to assess IL-33 effects on eosinophil behavior and hepatic stellate cell activation.
Significantly higher serum IL-33/ST-2 levels were found in AE patients compared to healthy controls (p < 0.05).
Increased IL-33/ST-2 expression was noted in close to lesion tissues versus distant tissues (p < 0.05).
Masson's trichrome staining indicated elevated fibrosis levels near the lesions.
IL-33 was shown to enhance eosinophil phagocytosis and migration, and upregulated α-SMA expression in hepatic stellate cells, especially with eosinophils present.

Abstract

Background: Alveolar echinococcosis (AE) is a serious zoonotic parasitic disease. This study aimed to investigate the mechanisms underlying the formation of the dense fibrotic band surrounding hepatic alveolar echinococcosis (HAE) lesions, which impedes chemotherapeutic drug penetration. Additionally, the roles of Interleukin-33 (IL-33) and eosinophils in the progression of fibrosis within this band were examined. Methods: IL-33/suppression of tumorigenicity 2 (ST-2) expression levels were compared between patients with HAE and healthy controls, as well as between close to lesion tissues (CLT) and distant from the lesion tissues (DLT) using enzyme-linked immunosorbent assay (ELISA), western blot, and immunohistochemistry. Immunofluorescence co-localization analysis was performed to examine IL-33/ST-2 and eosinophil distribution. Masson’s trichrome staining was used to evaluate fibrosis in AE lesions. Cellular assays were carried out to assess the effects of IL-33 on eosinophil phagocytosis and migration, as well as its impact on α-smooth muscle actin (α-SMA) expression in hepatic stellate cells (HSCs). Results: ELISA findings indicated significantly elevated serum IL-33/ST-2 levels in patients with AE compared with healthy controls (p < 0.05). Immunohistochemistry and western blot analyses demonstrated higher IL-33/ST-2 expression in CLT than in DLT (p < 0.05), with IL-33/ST-2 and eosinophils exhibiting a highly consistent distribution within CLT. Masson’s trichrome staining confirmed increased fibrosis in CLT. Cellular assays showed that IL-33 enhanced eosinophil phagocytosis and migration, while IL-33 stimulation upregulated α-SMA expression on the HSC surface, with this effect being more pronounced in the presence of eosinophils. Conclusion: IL-33 contributed to microenvironmental fibrosis within AE lesions via eosinophil-mediated mechanisms, highlighting a potential therapeutic target to improve chemotherapy efficacy in patients with AE.

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