Concurrent evaluation of oxidative stress biomarkers, cytokine expression, molecular identification, and histopathological findings in sheep naturally infected with Fasciola hepatica.

Ovine fascioliasis, caused by Fasciola species, challenges livestock productivity worldwide and remains insufficiently characterized at the molecular and immunological levels in endemic regions, such as Egypt. In 150 slaughtered sheep, the prevalence was determined, mitochondrial COX1 was sequenced for species identity, hepatic cytokine transcripts were quantified via qRT-PCR, oxidative stress biomarkers (MDA, TAC, TOS, and OSI) were assayed, and histopathology was evaluated. The prevalence was 15.3 %, with non-significant sex/season effects. COX1 phylogenetics confirmed that Fasciola hepatica identity was closely related to global haplotypes. Infected livers showed upregulation of pro-inflammatory (IL-1β) 4.0 × (, TNF-α) 6.6 × () and regulatory (IL-10 (5.3 ×), TGF-β (4.7 ×), and IL-4 (4.4 ×) cytokines, with downregulated IFN-γ (0.45 ×). Oxidative stress markers, including MDA (5 ×), TOS (6.1 ×), and OSI (3.6 ×), were significantly elevated, alongside a compensatory rise in TAC (7.8 ×). Histological examination revealed hepatocellular degeneration, bile duct hyperplasia, inflammatory infiltration, and fibrosis. These results elucidate the complex immune modulation and oxidative imbalance during F. hepatica infection and emphasize the necessity of integrated molecular and functional diagnostics to enhance fascioliasis management in sheep.