DATA OF A MODEL OF THE BLOOD-BRAIN BARRIER ON A CHIP DURING SEPSIS

Neuroinflammation plays a critical role in the pathogenesis of different neurological diseases, including sepsis which leads to neuronal damage. The blood-brain barrier critically participates in the modulation of NI, limiting the influx of inflammatory cells and mediators from the periphery to the Central Nervous System. Herein, a static blood-brain barrier on a chip model was developed using a native extracellular matrix membrane made of collagen I as cell culture surface, in which astrocytes, pericytes, microglia and endothelial cells were co-cultured. The BBBCh limited the diffusion of 10 and 40 kDa dextran/fluorescein and allows the expression of ZO-1, claudin-5 and nidogen. An inflamed BBBCh was mimicked using lipopolysaccharide that increased dextran/fluorescein permeability and diminished the expression of Clau-5. Dexamethasone administration reestablished the permeability and Clau-5 expression to their basal values. LPS administration mimicked the profile of a septic shock, by modifying the secretion of different cytokines, particularly TNF-α and IL-6 that were restored after Dexa administration. In summary, the developed platform is a useful tool to further study the physiopathology of the BBB under a NI status and will help to identify new anti-NI candidates.