Plasma membrane impacts of particulate matter on the blood-brain barrier

The potential for inhaled environmental particulate matter (PM) to cause neuronal effects is a growing concern, yet the underlying mechanisms remain unclear. There are two potential exposure routes via transport though the olfactory nerve transport and direct interaction of the circulating PM with the blood-brain barrier (BBB). This study investigated the plausible mechanism by which PM, once in circulation, could cross BBB's via the endotheliocytes, specifically focusing on the role of the plasma membrane. An in vitro BBB model (hCMEC/D3 cells) was exposed to ambient London PM (PM 10 , PM 2.5 ) and diesel exhaust particles (DEPs). Particle–membrane interactions were examined using focused ion beam scanning electron microscopy (FIB-SEM), confocal microscopy, and quasi-elastic neutron scattering (QENS). FIB-SEM revealed electron-dense, carbon-based particles interacting with the cellular models, with nanosized fractions showing pronounced plasma membrane associations. QENS data revealed significant changes in membrane dynamics following particle exposure. These findings suggest that direct interaction of PM with the endothelial membranes, facilitating particle uptake, and may represent a critical mechanism for PM exposure in the brain. • Impacts of PM 10 , PM 2.5 and DEPs on endotheliocyte plasma membrane were studied. • PM samples compromised cell membrane integrity concentration- and time-dependently. • FIB-SEM revealed nanoscale particles association with the plasma membrane. • Neutron scattering was employed to study endotheliocyte membrane dynamics. • QENS data showed significant changes in membrane dynamics post PM exposure.