Host transcriptional responses reveal molecular signatures of immune regulation and blood-brain barrier remodelling in porcine neurocysticercosis

Neurocysticercosis infection was associated with altered expression of genes involved in immune activation, together with reduced vascular- and endothelial-associated signalling. In contrast, anthelmintic treatment was associated with coordinated inflammatory and endothelial activation, including cell adhesion molecule pathways, extracellular matrix remodelling, and transcriptional features consistent with active blood-brain barrier remodelling in a disrupted lesion state.

Integrated pathway analysis showed that infection and treatment shared immune activation features but diverged in MAPK, vascular and endothelial programmes. These findings show that viable and post-treatment lesions are associated with distinct host transcriptional programmes involving immune regulation, endothelial activation and barrier-associated tissue remodelling. By defining these lesion-associated signatures, this study provides a framework for understanding parasite persistence, inflammation and disease progression in porcine neurocysticercosis.