{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Guimaraes AB"],"funding":["National Council for Scientific and Technological Development"],"pagination":["818"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12564545"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["47(10)"],"pubmed_abstract":["Cellular components and inflammatory mediators involved in the transmigration of HTLV-1-infected cells across the blood-brain barrier (BBB) are not fully understood. This study proposes a BBB model to identify the immunological mechanisms associated with HTLV-1 pathogenesis. PBMCs from individuals with HTLV-1-associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP) (<i>n</i> = 4) or HTLV-1-infected individuals without HAM/TSP (<i>n</i> = 4) were isolated. An indirect cell co-culture was performed between human brain microvascular endothelial (hBMEC) cells and neuroblastoma (SH-SY5Y) cells. PBMCs from healthy individuals (<i>n</i> = 4) were used as a negative control, and MT-2 cells were used as a positive control. Supernatants and cells were collected to quantify inflammatory cytokines and assess cell death after 24, 48, and 72 h. Multiple comparisons were performed using the Kruskal-Wallis test, followed by Fisher's LSD post hoc analysis. We observed that the production of cytokines IL-6, IL-8, IL-1β, TNF, IL-10, and IL-12p70, as well as the rate of neuronal death, was higher in co-cultures mimicking HAM/TSP carriers compared to HTLV-1-infected individuals without HAM/TSP and controls. Our results suggest that the HAM/TSP condition induces the release of IL-6, IL-8, IL-1β, TNF, IL-10, and IL-12p70, along with the infiltration of mononuclear cells, which may lead to neuronal death."],"journal":["Current issues in molecular biology"],"pubmed_title":["In Vitro Model of the Human Blood-Brain Barrier to Explore HTLV-1 Immunopathogenesis."],"pmcid":["PMC12564545"],"funding_grant_id":["400756/2019-6"],"pubmed_authors":["Morais C","Magalhaes P","Bernardo-Menezes L","Silva P","Cavalcante M","Agrelli A","Castellano LR","Vallinoto AC","Rodrigues C","Souza J","Azevedo E","Diniz G","Sena M","Gaiao WD","Guimaraes AB","Araujo Junior W"],"additional_accession":[]},"is_claimable":false,"name":"In Vitro Model of the Human Blood-Brain Barrier to Explore HTLV-1 Immunopathogenesis.","description":"Cellular components and inflammatory mediators involved in the transmigration of HTLV-1-infected cells across the blood-brain barrier (BBB) are not fully understood. This study proposes a BBB model to identify the immunological mechanisms associated with HTLV-1 pathogenesis. PBMCs from individuals with HTLV-1-associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP) (<i>n</i> = 4) or HTLV-1-infected individuals without HAM/TSP (<i>n</i> = 4) were isolated. An indirect cell co-culture was performed between human brain microvascular endothelial (hBMEC) cells and neuroblastoma (SH-SY5Y) cells. PBMCs from healthy individuals (<i>n</i> = 4) were used as a negative control, and MT-2 cells were used as a positive control. Supernatants and cells were collected to quantify inflammatory cytokines and assess cell death after 24, 48, and 72 h. Multiple comparisons were performed using the Kruskal-Wallis test, followed by Fisher's LSD post hoc analysis. We observed that the production of cytokines IL-6, IL-8, IL-1β, TNF, IL-10, and IL-12p70, as well as the rate of neuronal death, was higher in co-cultures mimicking HAM/TSP carriers compared to HTLV-1-infected individuals without HAM/TSP and controls. Our results suggest that the HAM/TSP condition induces the release of IL-6, IL-8, IL-1β, TNF, IL-10, and IL-12p70, along with the infiltration of mononuclear cells, which may lead to neuronal death.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Oct","modification":"2026-05-14T03:14:18.158Z","creation":"2026-05-14T03:08:59.547Z"},"accession":"S-EPMC12564545","cross_references":{"pubmed":["41150766"],"doi":["10.3390/cimb47100818"]}}