Moniezia benedeni infected Zaraibi (Egyptian Nubian) goats: Insights into serum biochemical changes, redox imbalance, and molecular mechanisms of oxidative-inflammatory cascades mediated intestinal injury.

Monieziosis caused by Moniezia spp. is an intestinal parasitic disease that deteriorates the health and productivity of small ruminants and may lead to death. This study aimed to estimate the monieziosis occurrence rate and its systemic impact in Zaraibi goats. Based on microscopic findings, molecular and phylogenetic analysis of the COX1 gene in Moniezia spp. infected goats (n = 380), twelve M. benedeni infected animals (MONZ, accession number OR053794) were enrolled in this study together with twelve healthy goats (Ctrl). The activities of hepatic (SA and SD), biliary (AP and γ-GT), and pancreatic (lipase and amylase) enzymes and the levels of globulin, T. Bilirubin, and creatinine were significantly increased (P ≤ 0.01) in the serum of infected goats. MONZ group displayed a significant increase in lipid profile (TC, TG, VLDL-C, and LDL-C, P ≤ 0.01) and a significant decrease in HDL-C (P ≤ 0.01) and PON-1(P ≤ 0.001). Positive APPs (CRP, haptoglobin, and α1-AGP) and proinflammatory cytokines (IL-33, IL-1β, and TNF-α) were significantly enhanced in the MONZ group. M. benedeni exacerbates a significant increase (P ≤ 0.001) of oxidative stress parameters (TOS, OSI, MDA, and GSSG) and a significant (P ≤ 0.001) consumption of the antioxidant defenses (TAS, SOD, CAT, GSH and GSH/GSSG). This oxidative burden mediates villous atrophy of enterocytes and Th2-biased immune response via the induction of TMED1/CD14+ mediated IL-33 signaling cascades, as well as LITAF-induced activation of TNF-α-dependent mRNA expression of NOX2-regulating subunit NCF4 pathway. This study clarified how M. benedeni could impair hepato-renal function, enterocyte integrity, redox signaling, and allergic inflammation-related genes at the intestinal tissue and systemic levels in goats.