GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE334nnn/GSE334289/primaryOK200TranscriptomicsSus scrofa domesticusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE334289GEOGSEfalseHost transcriptional responses reveal molecular signatures of immune regulation and blood-brain barrier remodelling in porcine neurocysticercosisNeurocysticercosis, caused by the establishment of Taenia solium larvae in the central nervous system, is a leading cause of acquired epilepsy and neurological morbidity in endemic regions. Viable cysticerci can persist in the brain for years with minimal inflammation, whereas parasite degeneration, either spontaneous or induced by antiparasitic treatment, triggers intense inflammatory and vascular responses. Despite the clinical relevance of this transition, the host transcriptional changes associated with viable infection and early post-treatment lesions remain poorly understood. We performed the first bulk RNA sequencing analysis of brain tissue from experimentally infected pigs, a physiologically relevant model of human neurocysticercosis. We compared transcriptional profiles from uninfected controls (n=3), infected untreated pigs with viable clear-capsule cysts (n=6), and infected pigs treated with albendazole plus praziquantel with disrupted blue-capsule lesions (n=3). Differential expression and pathway enrichment analyses were used to characterise host responses associated with infection and treatment. 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.2026/06/08GSE334289GSM9784640GSM9784638GSM9784639GSM9784634GSM9784635GSM9784636GSM9784637GSM9784641GSM9784642GSM9784643GSM9784633GSM978464429562334289Sus scrofa domesticus