ArticlePloS one2012
Exposure to lipopolysaccharide and/or unconjugated bilirubin impair the integrity and function of brain microvascular endothelial cells.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed.
- Postoperative neurocognitive disorder: migration and crosstalk of inflammation in the peripheral and central nervous system.Perioperative medicine (London, England) · 2026Review
- Implicating neuroinflammation in hippocampus, prefrontal cortex and amygdala with cognitive deficit: a narrative review.3 Biotech · 2025Review
- Unraveling the Vicious Cycle: Oxidative Stress and Neurotoxicity in Neurodegenerative Diseases.FASEB bioAdvances · 2025Review
- Biological attributes of zinc-dependent endopeptidases in endothelial dysfunction associated with sepsis: a narrative review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Peripheral Inflammation and Insulin Resistance: Their Impact on Blood-Brain Barrier Integrity and Glia Activation in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Phosphatidylserine induce thrombotic tendency and liver damage in obstructive jaundice.BMC gastroenterology · 2025Article
- Exploring the feasibility and clinical impact of ultrasound microvascular flow imaging in detecting brain injury in hyperbilirubinemia neonates.Scientific reports · 2025Article
- Maternal n-3 enriched diet reprograms the offspring neurovascular transcriptome and blunts inflammation induced by endotoxin in the neonate.Journal of neuroinflammation · 2024Article
- Geraniol attenuates oxygen-glucose deprivation/reoxygenation-induced ROS-dependent apoptosis and permeability of human brain microvascular endothelial cells by activating the Nrf-2/HO-1 pathway.Journal of bioenergetics and biomembranes · 2024Article
- Co-Culture Models: Key Players in In Vitro Neurotoxicity, Neurodegeneration and BBB Modeling Studies.Biomedicines · 2024Review
- TIMP-1 Protects Tight Junctions of Brain Endothelial Cells From MMP-Mediated Degradation.Pharmaceutical research · 2023Article
- Models of bilirubin neurological damage: lessons learned and new challenges.Pediatric research · 2023Review
- Serum Proteins Associated with Blood-Brain Barrier as Potential Biomarkers for Seizure Prediction.International journal of molecular sciences · 2022Article
- The Crosstalk between the Blood-Brain Barrier Dysfunction and Neuroinflammation after General Anaesthesia.Current issues in molecular biology · 2022Review
- Cerebral microvascular complications associated with SARS-CoV-2 infection: How did it occur and how should it be treated?Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Hsp90 inhibition protects brain endothelial cells against LPS-induced injury.BioFactors (Oxford, England) · 2022Article
- MyD88 Deficiency, but Not Gut Microbiota Depletion, Is Sufficient to Modulate the Blood-Brain Barrier Function in the Mediobasal Hypothalamus.Molecular neurobiology · 2022Article
- The blood-brain barrier in aging and neurodegeneration.Molecular psychiatry · 2022Review
- Addressing Blood-Brain Barrier Impairment in Alzheimer's Disease.Biomedicines · 2022Review
- A Breakdown of Immune Tolerance in the Cerebellum.Brain sciences · 2022Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSepsis and jaundice are common conditions in newborns that can lead to brain damage. Though lipopolysaccharide (LPS) is known to alter the integrity of the blood-brain barrier (BBB), little is known on the effects of unconjugated bilirubin (UCB) and even less on the joint effects of UCB and LPS on brain microvascular endothelial cells (BMEC). METHODOLOGY/PRINCIPAL
findingsMonolayers of primary rat BMEC were treated with 1 µg/ml LPS and/or 50 µM UCB, in the presence of 100 µM human serum albumin, for 4 or 24 h. Co-cultures of BMEC with astroglial cells, a more complex BBB model, were used in selected experiments. LPS led to apoptosis and UCB induced both apoptotic and necrotic-like cell death. LPS and UCB led to inhibition of P-glycoprotein and activation of matrix metalloproteinases-2 and -9 in mono-cultures. Transmission electron microscopy evidenced apoptotic bodies, as well as damaged mitochondria and rough endoplasmic reticulum in BMEC by either insult. Shorter cell contacts and increased caveolae-like invaginations were noticeable in LPS-treated cells and loss of intercellular junctions was observed upon treatment with UCB. Both compounds triggered impairment of endothelial permeability and transendothelial electrical resistance both in mono- and co-cultures. The functional changes were confirmed by alterations in immunostaining for junctional proteins β-catenin, ZO-1 and claudin-5. Enlargement of intercellular spaces, and redistribution of junctional proteins were found in BMEC after exposure to LPS and UCB.
conclusionsLPS and/or UCB exert direct toxic effects on BMEC, with distinct temporal profiles and mechanisms of action. Therefore, the impairment of brain endothelial integrity upon exposure to these neurotoxins may favor their access to the brain, thus increasing the risk of injury and requiring adequate clinical management of sepsis and jaundice in the neonatal period.
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