The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index; none of the 41 sources its claims cite is checked for support yet.
The Stressed CNS: When Glucocorticoids Aggravate Inflammation
Open accessAbstract
Glucocorticoids (GCs) are hormones released during the stress response that are well known for their immunosuppressive and anti-inflammatory properties; however, recent advances have uncovered situations wherein they have effects in the opposite direction. The CNS is a particularly interesting example, both because of its unique immune environment, and because GCs affect immune responses differently in different brain regions. In this minireview we discuss the contexts wherein GCs increase CNS inflammation and point out directions for future investigation.
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39 Not checked yet · 8 Own interpretation · 3 No basis given
In the paper
“indeed subacute stress induces GR-dependent microglia proliferation (Nair and Bonneau, 2006)”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Putative Mechanisms underlying the Inflammation-Enhancing Effects of GCs
What the sources say
- Not checked yetcites Nair and Bonneau, 2006
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“For example, acute stress 24 hr prior to lipopolysaccharide (LPS) treatment augments LPS-induced increases in plasma levels of IL-1β, TNF-α, and IL-6 (Johnson et al., 2002).”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Acute CORT Exposure Primes a Subsequent Inflammatory Response
What the sources say
- Not checked yetcites Johnson et al., 2002 source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“One mechanism to explain these endangering effects of CORT is that the hormone decreases glucose transport into neurons and glia in the hippocampus.”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Functional Implications: GCs Endanger Injured Neurons
What the sources say
- Not checked yetcites Sapolsky, 1999 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“GCs also decrease immune activation via protein-protein interactions between GR and NF-κB in the nucleus (Figure 1) (De Bosscher et al., 2003).”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > When GCs Are Immunosuppressive
What the sources say
- Not checked yetcites De Bosscher et al., 2003 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“In the absence of injury, acute stress can activate inflammatory mediators in the CNS.”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Stress and the Uninjured CNS
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“GC-augmented inflammation may also contribute to this endangerment.”
- Also stated in: § Functional Implications: GCs Endanger Injured Neurons · hedged
“The former conclusion is likely because GCs can augment LPS-induced CNS inflammation in the absence of neuronal death.”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Functional Implications: GCs Endanger Injured Neurons
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
- Also stated in: § Functional Implications: GCs Endanger Injured Neurons · hedged
In the paper
“indeed, impaired CORT secretion is implicated in several autoimmune disorders (Wick et al., 1993).”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > When GCs Are Immunosuppressive
What the sources say
- Not checked yetcites Wick et al., 1993
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“By contrast, acute stress post-LPS decreases the production of these same cytokines (Goujon et al., 1995).”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Acute CORT Exposure Primes a Subsequent Inflammatory Response
What the sources say
- Not checked yetcites Goujon et al., 1995 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Microglia are important in this response because when they are extracted from CORT pretreated rats and challenged ex vivo with LPS, they upregulate MHCII and toll-like receptor-4 (TLR-4) and produce more IL-1β and TNF-α than microglia extracted from control rats do (Frank et al., 2009).”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Acute CORT Exposure Has Priming Effects on Inflammation in the CNS
What the sources say
- Not checked yetcites Frank et al., 2009
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Reciprocally, MAPK (ERK and JNK) can decrease GR nuclear transport and affinity to cofactors via phosphorylation (Rogatsky et al., 1998).”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Putative Mechanisms underlying the Inflammation-Enhancing Effects of GCs
What the sources say
- Not checked yetcites Rogatsky et al., 1998 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 13
- Probably not a substantial claim. 1
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Both GCs and stress (in a GC-and GR-dependent manner) can augment aspects of inflammation in the CNS”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Conclusions
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As the key point, a class of stress hormones renowned for their capacity to suppress inflammation often fails to do so, and can even worsen inflammation in the injured CNS.”
- Also stated in: § Conclusions · plain
“GCs, while renowned for their anti-inflammatory actions, are not uniformly anti-inflammatory, including in the context of CNS inflammation.”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Abstract
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § Conclusions · plain
In the paper
“Basal CORT levels induce SHIP1, which increases NF-κB activation by inhibiting AKT (Zhang and Daynes, 2007).”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Putative Mechanisms underlying the Inflammation-Enhancing Effects of GCs
What the sources say
- Not checked yetcites Zhang and Daynes, 2007
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“This led to the theory that CORT secretion during stress actually mediates recovery from this initial immune activation (Munck et al., 1984).”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > When GCs Are Immunosuppressive
What the sources say
- Not checked yetcites Munck et al., 1984 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the 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).”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Functional Implications: GCs Endanger Injured Neurons
What the sources say
- Not checked yetcites Sapolsky and Pulsinelli, 1985
- Not checked yetcites Dinkel et al., 2003 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Moreover, subacute stress induces an increase in TNF-α levels in the cortex, and blocking this increase lessens stroke damage (Caso et al., 2006).”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Functional Implications: GCs Endanger Injured Neurons
What the sources say
- Not checked yetcites Caso et al., 2006 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Higher levels of CORT antagonize MAPK signaling by inducing expression of MAPK phosphatase-1 (MKP-1), which reduces NF-κB activation.”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Putative Mechanisms underlying the Inflammation-Enhancing Effects of GCs
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Acute stress increases NF-κB activity (Madrigal et al., 2001), intracellular TNF-α-convertase activity, extracellular TNF-α (Madrigal et al., 2002), and prostaglandin E2 and COX-2 levels (Madrigal et al., 2003) in the cortex.”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Stress and the Uninjured CNS
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“For example, chronic GC exposure reduces circulating leukocyte counts and decreases the production of a large variety of proinflammatory cytokines including IL-1β and TNF-α (De Bosscher et al., 2003).”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > When GCs Are Immunosuppressive
What the sources say
- Not checked yetcites De Bosscher et al., 2003 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Similarly, in cultured macrophages, CORT treatment 24 or 12 hr prior to LPS increases LPS-induced TNF-α, IL-6, and nitrite levels, while CORT treatment at 6, 3, or 0 hr prior to LPS does not (Smyth et al., 2004).”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Acute CORT Exposure Primes a Subsequent Inflammatory Response
What the sources say
- Not checked yetcites Smyth et al., 2004 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“For example, GR activation during chronic stress increases LPS-induced NF-κB activation and TNF-α, IL-1β, and iNOS expression in the hippocampus and frontal cortex, but has opposite effects in the hypothalamus (Munhoz et al., 2006).”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Brain Regional Differences in GC Effects
What the sources say
- Not checked yetcites Munhoz et al., 2006 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“CORT plays a role in this immune activation as well because basal levels of CORT are required for the synthesis of E in the adrenals (Wurtman and Axelrod, 1966) and for proper NE signaling (Joels and de Kloet, 1989).”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Basal GC Concentrations Are Required for Immune Activation
What the sources say
- Not checked yetcites Wurtman and Axelrod, 1966
- Not checked yetcites Joels and de Kloet, 1989 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“While there is widespread use of GCs in clinical neurology to control CNS inflammation in general and poststroke edema in particular, such interventions are often ineffective and can even worsen clinical outcome (Gomes et al., 2005).”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Conclusions
What the sources say
- Not checked yetcites Gomes et al., 2005 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In one study, microarray profiling demonstrates that while DEX can decrease human monocyte expression of many anti-inflammatory genes, it simultaneously increases the expression of a number of proinflammatory chemokines, complement proteins, and cytokines (Galon et al., 2002).”
§ The Stressed CNS: When Glucocorticoids Aggravate Inflammation > Putative Mechanisms underlying the Inflammation-Enhancing Effects of GCs
What the sources say
- Not checked yetcites Galon et al., 2002 source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
Findings from animal models of CNS inflammation and injury are relevant to human clinical neurology.
“Because of the obvious clinical implications of these findings, it is imperative to determine how GCs affect CNS inflammation, particularly when they make it worse.”
The paper relies on this without support.
LPS-induced CNS inflammation is a valid model for injury-induced CNS inflammation.
“Until now we have primarily considered situations wheren inflammation occurs in the absence of neuronal death (i.e., after LPS administration).”
Claims other papers make about this one
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In the citing paper
“Additionally, excess cortisol may increase the binding to Mineralocorticoid Receptors that can produce a pro-inflammatory response [23,24].”
From Chronic Stress and Autoimmunity: The Role of HPA Axis and Cortisol Dysregulation (2025) · cites this paper as [23]
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“This may lead to sustained production of pro-inflammatory cytokines like IL-6 and TNF-α [23].”
From Chronic Stress and Autoimmunity: The Role of HPA Axis and Cortisol Dysregulation (2025) · cites this paper as [23]
Experimental — accuracy not yet measured
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“This was true in both the brain and the liver, raising the possibility that chronic hypothalamic–pituitary–adrenal (HPA) axis activation (as may occur during chronic inflammation for example) exaccerbates inflammation in the brain and elsewhere (reviewed in Sorrells et al. (2009)).”
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“…response is a complex physiological mechanism and, although much of this mechanism has been unveiled in recent years (de Kloet et al., 2005; McEwen, 2010; Sorrells et al., 2009), the way whereby an incorrect stress response is linked to pathophysiology is still far from being completely understood.”
BackgroundPenninx, B. W., Milaneschi, Y., Lamers, F., & Vogelzangs, N. (2013) · BMC Medicine · doi:10.1186/1741-7015-11-129 · Cited by 839
“However, the relationship between HPA-activation and its effect on inflammation is extremely complex; whether glucocorticoids increase or decrease inflammation may depend on factors such as dose, duration and timing of glucocorticoids exposure and the brain area involved [134].”
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“Four-week chronic stress exposure significantly upregulates the inflammatory cytokines such as TNFα, IL-18, IL-1β and inflammatory inducible NOS (iNOS) expression (Peng et al., 2012).”
BackgroundInfluentialThe neurobiology of depression: An integrated view
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Metadata
- Authors
- Sorrells, S. F., Caso, J. R., Munhoz, C. D., & Sapolsky, R. M.
- Affiliations
- Stanford University (US)
- Stanford Medicine (US)
- Universidade de São Paulo (BR)
- Corresponding author
- Sorrells, Shawn F.
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2009-10
- Volume
- 64
- Issue
- 1
- Pages
- 33-39
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC4782919
- OpenAlex
- W2062298786
- Cited by
- 425
- References
- 52
- Citations by year
- 2026: 17 · 2025: 17 · 2024: 26 · 2023: 22 · 2022: 30 · 2021: 31 · 2020: 28 · 2019: 20 · 2018: 34 · 2017: 29 · 2016: 19 · 2015: 27 · 2014: 35 · 2013: 22 · 2012: 28
- FWCI
- 1.22
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (R01NS059918, F31NS063491)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- glucocorticoids, neuroinflammation, stress response, neuroendocrine-immune interaction
- MeSH terms
- Animals, Brain, Encephalitis, Glucocorticoids, Humans, Inflammation, Models, Neurological, Myelitis, Neurons, Spinal Cord, Stress, Physiological, Neuroimmunomodulation
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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.
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