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    <responseDate>2026-10-14T15:04:43Z</responseDate>
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    <identifier>10.57760/sciencedb.20290</identifier>
    <datestamp>2025-01-26T20:01:09Z</datestamp>
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  <dc:date>2025-01-26</dc:date>
  <dc:title>DATA OF A MODEL OF THE BLOOD-BRAIN BARRIER ON A CHIP DURING SEPSIS</dc:title>
  <dc:identifier>doi:10.57760/sciencedb.20290</dc:identifier>
  <dc:language>en</dc:language>
  <dc:description>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.&amp;nbsp;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-&amp;alpha; 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.&amp;nbsp; </dc:description>
  <dc:subject>Blood-brain barrier; Organ-on-a-chip; neuroinflammation; dexamethasone; sepsis.</dc:subject>
  <dc:creator>Iván Nicolás Pérez Osorio</dc:creator>
  <dc:rights>PUBLIC</dc:rights>
  <dc:rights>https://creativecommons.org/licenses/by/4.0/</dc:rights>
  <dc:type>dataset</dc:type>
  <dc:publisher>Science Data Bank</dc:publisher>
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