Cyclooxygenase 2 (COX-2) inhibition increases the inflammatory response in the brain during systemic immune stimuli
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Non-steroidal anti-inflammatory drugs (NSAIDs) and inhibitors of the cyclooxygenase (COX) pathways are currently recommended for the prevention and treatment of several inflammatory diseases, including neurodegenerative disorders. However non-selective blockade of COX was found to have pro-inflammatory properties, because they have the ability to alter the plasma glucocorticoid levels that play a critical role in the control of the innate immune response. The present study investigated the role of non-selective (ketorolac or indomethacin) or specific inhibitors of COX-1 (SC-560) and COX-2 (NS-398) in these effects. Mice challenged systemically with the endotoxin lipopolysaccharide (LPS) exhibited a robust hybridization signal for numerous inflammatory genes in vascular-associated cells of the brain and microglia across the cerebral tissue. Ketorolac, indomethacin and NS-398 significantly increased the ability of LPS to trigger such an innate immune response at time 3 h post challenge, whereas SC-560 failed to change gene expression in the brain of animals treated with the endotoxin. These data together with the crucial role of COX-2-derived prostaglandin E2 (PGE2) in the increase of glucocorticoids during systemic immune stimuli provide evidence that inhibition of this pathway results in an exacerbated early innate immune reaction. This may have a major impact on the use of these drugs in diseases where inflammation is believed to be a contributing and detrimental factor.
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The effect of COX inhibitors on NF-kappaB target genes could be replicated by administration of the GR antagonist RU486.
“Interestingly, this effect could be replicated by the administration of the GR antagonist RU486 (mifepristone) (135, 136).”
From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [136]
Non-selective COX inhibitors ketorolac and indomethacin potentiate the expression of NF-kappaB target genes in brain capillaries and parenchymal microglia during systemic inflammation by hampering activation of the HPA axis and subsequent release of GCs.
“Complementarily, the non-selective COX inhibitors ketorolac and indomethacin were found to potentiate the expression of NF-κB target genes in brain capillaries and parenchymal microglia during systemic inflammation (i.v. bolus of LPS, IL-1β, or TNF-α) by hampering the activation of the HPA axis and the subsequent release of GCs.”
From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [136]
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Selective COX-2 Inhibitors as Neuroprotective Agents in Traumatic Brain Injury
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- Authors
- Blais, V., Turrin, N. P., & Rivest, S.
- Affiliations
- Centre hospitalier de l'Université Laval (CA)
- ORCID
- Rivest, Serge
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2005-11-08
- Volume
- 95
- Issue
- 6
- Pages
- 1563-1574
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2002245685
- Cited by
- 72
- References
- 56
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 3 · 2022: 1 · 2021: 3 · 2020: 4 · 2019: 1 · 2018: 2 · 2017: 10 · 2015: 5 · 2014: 2 · 2013: 2 · 2012: 4
- FWCI
- 3.40
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Université Laval
- Canada Research Chairs
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
- Keywords
- COX-2 inhibition, cyclooxygenase-2, nonsteroidal anti-inflammatory drugs, ketorolac, indomethacin, SC-560, NS-398, lipopolysaccharide, innate immune response, microglia, neuroinflammation, glucocorticoids, prostaglandin E2, neurodegenerative diseases
- MeSH terms
- Prostaglandin-E Synthases, Animals, Blood-Brain Barrier, Brain, Indomethacin, Inflammation, Lipopolysaccharides, Male, Nitrobenzenes, Plasmids, Pyrazoles, Sulfonamides, Dinoprostone, Gene Expression, Cyclooxygenase Inhibitors, In Situ Hybridization, Intramolecular Oxidoreductases, Ketorolac, Mice, Cyclooxygenase 1, Cyclooxygenase 2 Inhibitors
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