Lipopolysaccharide-induced blood-brain barrier disruption: Roles of cyclooxygenase, oxidative stress, neuroinflammation, and elements of the neurovascular unit
Open accessAbstract
BACKGROUND: Disruption of the blood-brain barrier (BBB) occurs in many diseases and is often mediated by inflammatory and neuroimmune mechanisms. Inflammation is well established as a cause of BBB disruption, but many mechanistic questions remain. METHODS: We used lipopolysaccharide (LPS) to induce inflammation and BBB disruption in mice. BBB disruption was measured using (14)C-sucrose and radioactively labeled albumin. Brain cytokine responses were measured using multiplex technology and dependence on cyclooxygenase (COX) and oxidative stress determined by treatments with indomethacin and N-acetylcysteine. Astrocyte and microglia/macrophage responses were measured using brain immunohistochemistry. In vitro studies used Transwell cultures of primary brain endothelial cells co- or tri-cultured with astrocytes and pericytes to measure effects of LPS on transendothelial electrical resistance (TEER), cellular distribution of tight junction proteins, and permeability to (14)C-sucrose and radioactive albumin. RESULTS: In comparison to LPS-induced weight loss, the BBB was relatively resistant to LPS-induced disruption. Disruption occurred only with the highest dose of LPS and was most evident in the frontal cortex, thalamus, pons-medulla, and cerebellum with no disruption in the hypothalamus. The in vitro and in vivo patterns of LPS-induced disruption as measured with (14)C-sucrose, radioactive albumin, and TEER suggested involvement of both paracellular and transcytotic pathways. Disruption as measured with albumin and (14)C-sucrose, but not TEER, was blocked by indomethacin. N-acetylcysteine did not affect disruption. In vivo, the measures of neuroinflammation induced by LPS were mainly not reversed by indomethacin. In vitro, the effects on LPS and indomethacin were not altered when brain endothelial cells (BECs) were cultured with astrocytes or pericytes. CONCLUSIONS: The BBB is relatively resistant to LPS-induced disruption with some brain regions more vulnerable than others. LPS-induced disruption appears is to be dependent on COX but not on oxidative stress. Based on in vivo and in vitro measures of neuroinflammation, it appears that astrocytes, microglia/macrophages, and pericytes play little role in the LPS-mediated disruption of the BBB.
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Lipopolysaccharide disrupts the blood-brain barrier by increasing permeability, thereby increasing the impact of circulating cytokines on central appetite regulation.
“LPS disrupts the blood–brain barrier (i.e., increases permeability) [41] to increase the impact of circulating cytokines on central appetite regulation;”
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- Authors
- Banks, W. A., Gray, A. M., Erickson, M. A., Salameh, T. S., Damodarasamy, M., Sheibani, N., Meabon, J. S., Wing, E. E., Morofuji, Y., Cook, D. G., & Reed, M. J.
- Affiliations
- University of Washington (US)
- VA Puget Sound Health Care System (US)
- University of Wisconsin–Madison (US)
- University of Nagasaki (JP)
- Corresponding author
- Banks, William A.
- ORCID
- Venue
- Journal of Neuroinflammation
- Published
- 2015-11-25
- Volume
- 12
- Issue
- 1
- Pages
- 223-223
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC4660627
- OpenAlex
- W2175869408
- Cited by
- 636
- References
- 61
- Citations by year
- 2026: 81 · 2025: 56 · 2024: 75 · 2023: 59 · 2022: 78 · 2021: 79 · 2020: 79 · 2019: 39 · 2018: 48 · 2017: 25 · 2016: 15 · 2015: 1 · 2012: 1
- FWCI
- 15.82
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion, cc-by-nc-nd)
- Nagasaki University's Academic Output SITE (Nagasaki University) (submittedVersion, cc-by-nc-nd)
- Funders
- va
- National Institutes of Health (AG029839)
- Topics
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Keywords
- blood-brain barrier disruption, lipopolysaccharide, cyclooxygenase, indomethacin, oxidative stress, neuroinflammation, neurovascular unit, astrocytes, microglia/macrophages, pericytes, brain endothelial cells, tight junctions, regional brain vulnerability, neuroimmune mechanisms
- MeSH terms
- Animals, Astrocytes, Blood-Brain Barrier, Cell Line, Transformed, Dose-Response Relationship, Drug, Inflammation, Lipopolysaccharides, Male, Prostaglandin-Endoperoxide Synthases, Oxidative Stress, Inflammation Mediators, Coculture Techniques, Endothelial Cells, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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