The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.
Novel glucocorticoid effects on acute inflammation in the CNS
Abstract
The CNS can mount an inflammatory reaction to excitotoxic insults that contributes to the emerging brain damage. Therefore, anti-inflammatory drugs should be beneficial in neurological insults. In contrast, glucocorticoids (GCs), while known for their anti-inflammatory effects, can exacerbate neurotoxicity in the hippocampus after excitotoxic insults. We investigated the effect of GCs on the inflammatory response after a neurological insult. Intact control (INT; intact stress response GC profile), adrenalectomized/GC-supplemented (ADX; low basal GC profile) and GC-treated (COR; chronically high GC profile) rats were injected with kainic acid into the hippocampal CA3 region. Lesion size was determined 8-72 h later. The inflammatory response was characterized using immunohistochemistry, RNAse protection assay and ELISA. The INT and COR rats developed larger CA3 lesions than ADX rats. We found that GCs surprisingly caused an increase in relative numbers of inflammatory cells (granulocytes, monocytes/macrophages and microglia). Additionally, mRNA and protein (IL-1beta and TNF-alpha) levels of the pro-inflammatory cytokines IL-1alpha, IL-1beta and TNF-alpha were elevated in COR rats compared with INT and ADX rats. These data strongly question the traditional view of GCs being uniformly anti-inflammatory and could further explain how GCs worsen the outcome of neurological insults.
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In the citing paper
“Yet, there are exceptions – pro-inflammatory effects of glucocorticoids that depend on dose and cell or tissue type (Dinkel et al., 2003; MacPherson et al., 2005).”
From Central effects of stress hormones in health and disease: understanding the protective and damaging effects of stress and stress mediators (2008) · cites this paper as Dinkel et al., 2003
In the citing paper
“Yet, there are exceptions - proinflammatory effects of glucocorticoids that depend on dose and cell or tissue type.6,7”
From Protective and damaging effects of stress mediators: central role of the brain (2006) · cites this paper as [6]
In the citing paper
“Subacute CORT treatment increases inflammatory cell recruitment and cytokine production at an excitotoxic injury site (Dinkel et al., 2003).”
From The Stressed CNS: When Glucocorticoids Aggravate Inflammation (2009) · cites this paper as Dinkel et al., 2003
In the citing paper
“This was seen in one study where GCs increased inflammatory cell infiltration prior to the emergence of neuronal death (Dinkel et al., 2003).”
From The Stressed CNS: When Glucocorticoids Aggravate Inflammation (2009) · cites this paper as Dinkel et al., 2003
In the citing paper
“For example, subacute CORT treatment worsens CA1 hippocampal neuron loss caused by global ischemia (Sapolsky and Pulsinelli, 1985) and CA3 neuron loss caused by excitotoxins (Dinkel et al., 2003).”
From The Stressed CNS: When Glucocorticoids Aggravate Inflammation (2009) · cites this paper as Dinkel et al., 2003
Citations
Cites
Microglia: a sensor for pathological events in the CNS
Kreutzberg, G. W. (1996) · Trends in Neurosciences · doi:10.1016/0166-2236(96)10049-7 · Cited by 4,396
Pathobiology of ischaemic stroke: an integrated view
Dirnagl, U., Iadecola, C., & Moskowitz, M. A. (1999) · Trends in Neurosciences · doi:10.1016/s0166-2236(99)01401-0 · Cited by 3,943
Physiological functions of glucocorticoids in stress and their relation to pharmacological actions
MUNCK, A., GUYRE, P. M., & HOLBROOK, N. J. (1984) · Endocrine Reviews · doi:10.1210/edrv-5-1-25 · Cited by 3,083
Excitatory Amino Acids as a Final Common Pathway for Neurologic Disorders
Epstein, F. H., Lipton, S. A., & Rosenberg, P. A. (1994) · New England Journal of Medicine · doi:10.1056/nejm199403033300907 · Cited by 2,676
Immunoregulatory Feedback Between Interleukin-1 and Glucocorticoid Hormones
Besedovsky, H., del Rey, A., Sorkin, E., & Dinarello, C. A. (1986) · Science · doi:10.1126/science.3014662 · Cited by 1,519
Adrenal steroid receptors and actions in the nervous system
McEwen, B. S., de Kloet, E. R., & Rostène, W. H. (1986) · Physiological Reviews · doi:10.1152/physrev.1986.66.4.1121 · Cited by 1,238
Corticotropin-releasing factor-producing neurons in the rat activated by interleukin-1
Berkenbosch, F., van Oers, J., del Rey, A., Tilders, F., & Besedovsky, H. (1987) · Science · doi:10.1126/science.2443979 · Cited by 1,151
The changing landscape of ischaemic brain injury mechanisms
Lee, J.-M., Zipfel, G. J., & Choi, D. W. (1999) · Nature · doi:10.1038/399a007 · Cited by 1,102
Banati, R. B., Gehrmann, J., Schubert, P., & Kreutzberg, G. W. (1993) · Glia · doi:10.1002/glia.440070117 · Cited by 1,032
Research works printed but not linked: 1
- Millikan C., 1987, Stroke, 117
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Physiology and neurobiology of stress and adaptation: central role of the brain
McEwen, B. S. (2007) · Physiological Reviews · doi:10.1152/physrev.00041.2006 · Cited by 5,429
McEwen, B. S. (2008) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2007.11.071 · Cited by 1,864
Protective and damaging effects of stress mediators: central role of the brain
McEwen, B. S. (2006) · Dialogues in Clinical Neuroscience · doi:10.31887/dcns.2006.8.4/bmcewen · Cited by 1,220
Brain Inflammation in Epilepsy: Experimental and Clinical Evidence
Vezzani, A., & Granata, T. (2005) · Epilepsia · doi:10.1111/j.1528-1167.2005.00298.x · Cited by 1,049
Ravizza, T., Gagliardi, B., Noè, F. M., Boer, K., Aronica, E., & Vezzani, A. (2007) · Neurobiology of Disease · doi:10.1016/j.nbd.2007.08.012 · Cited by 700
Metadata
- Authors
- Dinkel, K., MacPherson, A., & Sapolsky, R. M.
- Affiliations
- Stanford University (US)
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2003-01-31
- Volume
- 84
- Issue
- 4
- Pages
- 705-716
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W1538656778
- Cited by
- 179
- References
- 52
- Citations by year
- 2025: 2 · 2024: 4 · 2023: 5 · 2022: 7 · 2021: 9 · 2020: 9 · 2019: 3 · 2018: 3 · 2017: 3 · 2016: 8 · 2015: 7 · 2014: 12 · 2013: 9 · 2012: 7
- FWCI
- 6.35
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (2r01mh053814-04)
- National Institute of Mental Health (R01 MH 53814)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- glucocorticoids, acute inflammation, central nervous system, excitotoxicity, kainic acid, hippocampus, neuroinflammation, adrenalectomy, stress response, inflammatory cytokines, IL-1β, TNF-α, microglia, macrophages, granulocytes, neurotoxicity
- MeSH terms
- Acute Disease, Adrenalectomy, Animals, Cell Count, Encephalomyelitis, Glucocorticoids, Granulocytes, Hippocampus, Interleukin-1, Kainic Acid, Macrophages, Male, RNA, Messenger, Steroids, Tumor Necrosis Factor-alpha, Cytokines, Rats, Sprague-Dawley, Microglia, Excitatory Amino Acid Agonists, Rats
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