INTRODUCTION: Nanoplastics (NPs) are emerging contaminants that can cross biological barriers and accumulate in the CNS. Increasing evidence indicates that BBB dysfunction and neuroinflammation are early events in neurodegenerative disorders. However, the combined impact of NPs and inflammatory stimuli on human neurovascular cells remains insufficiently characterized.

AIM(S): We hypothesized that NPs potentiate LPS-induced inflammatory responses in human brain endothelial (HBEC-5i) and astroglial cells, thereby promoting neurovascular dysfunction.

METHOD(S): HBEC-5i and astrocyte cells were exposed to NPs, LPS, or a combination. Cell metabolic activity and viability were assessed using MTT and NRU assays, proliferative capacity was evaluated by BrdU test. Quantitative PCR was performed to assess selected inflammatory markers. All experiments were conducted under controlled in vitro conditions with appropriate controls.

RESULTS: Preliminary analyses indicate that exposure to NP+LPS induced more pronounced alterations in cellular metabolic activity and proliferation than single treatments. Notably, MTT and NRU assays showed an altered metabolic response under co-exposure conditions. BrdU incorporation assays demonstrated treatment-dependent modulation of proliferative activity. Gene expression analysis revealed treatment-dependent changes in pro-inflammatory markers, most pronounced in the NP+LPS group.

CONCLUSIONS: Our findings suggest that NPs may amplify inflammation-related responses in both cell types, particularly under conditions of concomitant immune activation. We observed additive effects of NP and LPS exposure, supporting the concept that NPs could exacerbate neuroinflammatory

FINANCIAL SUPPORT: The project is financed from the state budget, allocated by the Minister of Science and Higher Education under the "Student science clubs create innovations" program.