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Schistosomiasis can lead to vascular damage resulting in pulmonary arterial hypertension (PAH). Although its pathophysiology remains unclear, cytokine imbalance is known to play a key role. This study aimed to evaluate serum mediators in association with hemodynamic, echocardiographic, and histological parameters in a murine model of Schistosoma mansoni-induced pulmonary hypertension (Sch-PH). Twenty male C57BL/6 mice were randomized into infected group and non-infected control group. Sch-PH was induced by intraperitoneal inoculation of S. mansoni eggs (240 eggs/g body weight), followed by intravenous administration (175 eggs/g). After 21 days, systolic pulmonary artery pressure was measured by right ventricular catheterization (RHC), and cardiac function was assessed by transthoracic echocardiography. Animals were then euthanized for collection of lungs and heart for histopathology, and blood samples were obtained for quantification of interleukin (IL)-6, IL-10, and tumor necrosis factor (TGF)-β1 by ELISA. The Sch-PH group had significantly lower tricuspid annular plane systolic excursion and pulmonary artery acceleration time/pulmonary ejection time ratio (P<0.05), and increased pulmonary artery peak flow, tricuspid and pulmonary regurgitation, IL-6, and TGF-β1 levels (P<0.05). IL-10 was undetectable. Lung tissue showed inflammatory infiltrates, alveolar and perivascular granulomas, and S. mansoni eggs. Pulmonary arteries exhibited intimal thickening, medial hypertrophy, and fibrosis. Cardiac tissue presented inflammatory foci, fibroblast proliferation, and thickening of connective septa. IL-6 and TGF-β1 were elevated in Sch-PH and correlated with echocardiographic and hemodynamic alterations. These findings suggest a role for these mediators in Sch-PH pathogenesis and highlight the potential for targeting inflammatory pathways in this condition.