Investigates the link between hydatid infection and lung cancer in sheep, suggesting immune modulation roles.
Background: Pulmonary hydatidosis infection, caused by Echinococcus granulosus larvae, is a zoonotic disease that stimulates remarkable histological and immunological alterations in infected host tissues.Objectives: This study investigated the link between hydatid infection and alveolar adenocarcinoma in sheep lungs, alongside the localized immune response, including CD4+ and CD8+ T cells and PD-L1 expression. Methods: A total of 24 hydatid-infected and 10 non-infected ovine lung samples were examined using histopathological (H&E, PAS, Masson’s trichrome) and immunohistological (CD4, CD8, and PD-L1) techniques. Results: Results demonstrated that 36% of infected lungs revealed adenocarcinoma, accompanied by notable inflammation, necrosis, and fibrosis. Immunohistological tests demonstrated an increase in CD4+ and CD8+ T-cell infiltration in infected tissues, with PD-L1 expression significantly higher in adenocarcinoma-associated samples compared to non-infected and hydatid-only lungs. Conclusion: These results suggest that chronic hydatid infection may contribute to oncogenic transformation through modulation of immune response, particularly via exhaustion of PD-L1-mediated T-cells. This study also highlights the possible role of E. granulosus in pulmonary carcinogenesis and emphasizes the importance role of immune checkpoint molecules in parasitic and neoplastic evasion mechanisms.
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Farhan et al. (2026) studied this question.
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