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.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
0 of 41 cited sources checked · 0 supported · 0 flagged
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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn 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
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes
- 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source doesn’t support the claim as written.
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
Citations
Cites
(2005) · Choice Reviews Online · doi:10.5860/choice.43-0626 · Cited by 4,726
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
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
Brain corticosteroid receptor balance in health and disease
de Kloet, E. R., Vreugdenhil, E., Oitzl, M. S., & Joëls, M. (1998) · Endocrine Reviews · doi:10.1210/edrv.19.3.0331 · Cited by 2,614
The IκB-NF-κB Signaling Module: Temporal Control and Selective Gene Activation
Hoffmann, A., Levchenko, A., Scott, M. L., & Baltimore, D. (2002) · Science · doi:10.1126/science.1071914 · Cited by 1,890
Dhabhar, F. S., & McEwen, B. S. (1997) · Brain Behavior and Immunity · doi:10.1006/brbi.1997.0508 · Cited by 1,014
De Bosscher, K., Vanden Berghe, W., & Haegeman, G. (2003) · Endocrine Reviews · doi:10.1210/er.2002-0006 · Cited by 898
McEwen, B. S., Biron, C. A., Brunson, K. W., Bulloch, K., Chambers, W. H., Dhabhar, F. S., Goldfarb, R. H., Kitson, R. P., Miller, A. H., Spencer, R. L., et al. (1997) · Brain Research Reviews · doi:10.1016/s0165-0173(96)00012-4 · Cited by 837
Karst, H., Berger, S., Turiault, M., Tronche, F., Schütz, G., & Joëls, M. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0507572102 · Cited by 774
Glucocorticoids Potentiate Ischemic Injury to Neurons: Therapeutic Implications
Sapolsky, R. M., & Pulsinelli, W. A. (1985) · Science · doi:10.1126/science.4035356 · Cited by 678
Self-citation
Flagged first, then by citations
Cited by
Sorted by citations
Items 201–300 of 426
Nikkheslat, N., Pariante, C. M., & Zunszain, P. A. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-811073-7.00003-9 · Cited by 23
Familial Mediterranean fever: the molecular pathways from stress exposure to attacks
Korkmaz, C., Cansu, D. Ü., & Cansu, G. B. (2020) · Rheumatology · doi:10.1093/rheumatology/keaa450 · Cited by 23
Niemegeers, P., Boer, P. D., Dumont, G., Eede, F. V. D., Fransén, E., Claes, S. J., Morrens, M., & Sabbe, B. (2016) · Neuropsychobiology · doi:10.1159/000466698 · Cited by 21
“However, recent evidence shows that glucocorticoids are not exclusively anti-inflammatory, and can, in certain contexts, enhance pro-inflammatory responses, possibly through microglia activation, which is associated with psychiatric disorders including major depressive disorder (34, 35).”
Animal Models of Early-Life Adversity
Benmhammed, H., Hayek, S. E., Berkik, I., Mostafi, H. E., Bousalham, R., Mesfioui, A., Ouichou, A., & Hessni, A. E. (2019) · Methods in molecular biology · doi:10.1007/978-1-4939-9554-7_10 · Cited by 27
Glucocorticoids can arm macrophages for innate immune battle
Sorrells, S. F., & Sapolsky, R. M. (2009) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2009.10.004 · Cited by 21
Self-citationSteroid-Induced Sleep Disturbance and Delirium: A Focused Review for Critically Ill Patients
Cole, J. L. (2020) · Federal Practitioner · doi:10.12788/fp.003 · Cited by 20
Sedaghat, K., Naderian, R., Pakdel, R., Bandegi, A., & Ghods, Z. (2021) · Molecular Biology Reports · doi:10.1007/s11033-021-06810-2 · Cited by 21
Miró‐Mur, F., Laredo, C., Renú, A., Rudilosso, S., Zhao, Y., Amaro, S., Llull, L., Urra, X., Planas, A. M., & Chamorro, Á. (2018) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2018.03.018 · Cited by 20
“…cortex suppresses the production of pro-inflammatory mediators (Wilckens and De Rijk, 1997). and facilitates the release of anti-inflammatory molecules (Barrat et al., 2002), although available evidence also reveals situations where cortisol actually increases inflammation (Sorrells et al., 2009).”
BackgroundInnate Immunity and Glucocorticoids: Potential Regulatory Mechanisms in Epididymal Biology
Silva, E. J. R., Queiróz, D. B. C., Rodrigues, A. M. T., Honda, L., & Avellar, M. C. W. (2011) · Journal of Andrology · doi:10.2164/jandrol.111.013565 · Cited by 19
Heart, Brain and Mental Health Disparities for LGBTQ People of Color
(2021) · Springer eBooks · doi:10.1007/978-3-030-70060-7 · Cited by 17
Glannon, W. (2018) · doi:10.1093/med/9780198758853.001.0001 · Cited by 29
Robledo‐Montaña, J., Díaz-García, C., Martínez, M., Ambrosio, N., Montero, E., Marín, M. J., Virto, L., Muñoz‐López, M., Herrera, D., Sanz, M., et al. (2024) · Journal of Neuroinflammation · doi:10.1186/s12974-024-03213-5 · Cited by 19
Bollaerts, I., houcke, J. V., Beckers, A., Lemmens, K., Vanhunsel, S., Groef, L. D., & Moons, L. (2019) · Mediators of Inflammation · doi:10.1155/2019/6135795 · Cited by 18
Elucidating the Complex Interactions between Stress and Epileptogenic Pathways
Friedman, A. R., Cacheaux, L. P., Ivens, S., & Kaufer, D. (2011) · Cardiovascular Psychiatry and Neurology · doi:10.1155/2011/461263 · Cited by 17
“For example, early life stress is detrimental by many metrics, but may also lead to a blunting of inflammatory response that is protective in terms of epilepsy vulnerability [60].”
Haavik, H., Niazi, I. K., Kumari, N., Amjad, I., Duehr, J., & Holt, K. R. (2021) · Medicina · doi:10.3390/medicina57060536 · Cited by 19
Newbury, J. B., Arseneault, L., Moffitt, T. E., Odgers, C. L., Howe, L. D., Bakolis, I., Reuben, A., Danese, A., Sugden, K., Williams, B. S., et al. (2023) · Schizophrenia Bulletin · doi:10.1093/schbul/sbad017 · Cited by 20
The Role of the Adrenal–Gut–Brain Axis on Comorbid Depressive Disorder Development in Diabetes
Mázala-de-Oliveira, T., da Silva, B. P. B., Campello‐Costa, P., & Carvalho, V. F. (2023) · Biomolecules · doi:10.3390/biom13101504 · Cited by 19
Dankel, S. J., Loenneke, J. P., & Loprinzi, P. D. (2016) · International Journal of Behavioral Medicine · doi:10.1007/s12529-016-9541-3 · Cited by 19
Wang, N., Ma, H., Li, Z., Gao, Y., Cao, X., Jiang, Y., Zhou, Y., & Liu, S. (2017) · PLoS ONE · doi:10.1371/journal.pone.0183077 · Cited by 18
Munk, A., Reme, S. E., & Jacobsen, H. B. (2021) · Frontiers in Psychology · doi:10.3389/fpsyg.2021.630422 · Cited by 16
“In the perioperative phase, breast cancer patients often experience high levels of distress and expect a variety of post-surgery symptoms (Deane and Degner, 1998; Spencer et al., 1999).”
BackgroundChronic stress as an emerging risk factor for the development and progression of glioma
Yi, L., Lin, X., She, X., Gao, W. Q., & Wu, M. (2024) · Chinese Medical Journal · doi:10.1097/cm9.0000000000002976 · Cited by 16
“[66,67] Dysregulated vagal inhibition is also observed in CS, whereby the cholinergic anti-inflammatory pathways acting via the vagal nerve are inhibited, resulting in reduced release of anti-inflammatory cytokines and an increase in inflammation in the body.”
BackgroundGlucocorticoids and nervous system plasticity
Lerch, J. K., & Madalena, K. M. (2016) · Neural Regeneration Research · doi:10.4103/1673-5374.175039 · Cited by 16
Freiman, S. V., Onufriev, M. V., Stepanichev, M. Y., Moiseeva, Y. V., Лазарева, Н. А., & Gulyaeva, N. V. (2016) · Neurochemical Journal · doi:10.1134/s1819712416020033 · Cited by 16
Matsumoto, Y., Niwa, M., Mouri, A., Noda, Y., Fukushima, T., Ozaki, N., & Nabeshima, T. (2017) · Psychopharmacology · doi:10.1007/s00213-017-4704-8 · Cited by 15
“Psychological stress activates the hypothalamic-pituitaryadrenal (HPA) axis and induces production of glucocorticoids in the adrenals, which can trigger psychiatric conditions (Axelrod and Reisine 1984; Joels and Baram 2009; Sorrells et al. 2009).”
Chen, H. C., Spiers, J. G., Sernia, C., & Lavidis, N. A. (2018) · The International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyy033 · Cited by 16
“…important adaptive action by glucocorticoids, with dissipation of the fight/flight response heightening immune defences and vigilance beyond basal levels and promoting more vigorous reactions to persisting or impending threats (Sapolsky et al., 2000; Johnson et al., 2002; Sorrells et al., 2009).”
BackgroundCortisol levels are influenced by sedation in the acute phase after subarachnoid haemorrhage
LINDGREN, C., Dahlqvist, P. M., Lindvall, P., Nilsson, L. M., Koskinen, L., & Naredi, S. (2012) · Acta Anaesthesiologica Scandinavica · doi:10.1111/aas.12014 · Cited by 13
Tobar, I. D. B., Fernández, P., Sáez, J. C., & Dagnino‐Subiabre, A. (2021) · Journal of Neuroscience Research · doi:10.1002/jnr.24902 · Cited by 16
“Although it remains to be determined whether GCs induce CRF release in these interneurons as they do in CRF neurons of the hypothalamus (Sorrells et al., 2009), it can be proposed that a mechanism similar to that described above could explain the increase in membrane permeability found in microglia…”
BackgroundBoero, G., Tyler, R., O'Buckley, T., Balan, I., Besheer, J., & Morrow, A. (2022) · Biomolecules · doi:10.3390/biom12081134 · Cited by 14
“However, in the past decades, several studies proved that glucocorticoids have also a pro-inflammatory impact on immune system [56,57].”
BackgroundGuijarro, I. M., Garcés, M., Andrés‐Benito, P., Marín, B., Otero, A., Barrio, T., Carmona, M., Ferrer, I., Badiola, J. J., & Monzón, M. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21093231 · Cited by 15
Niwa, M., Lockhart, S., Wood, D. J., Yang, K., de Oliveira, J. F., Kin, K., Ahmed, A., Wand, G. S., Kano, S., Payne, J. L., et al. (2024) · Nature Mental Health · doi:10.1038/s44220-024-00217-1 · Cited by 19
Review: Effects of Ractopamine Hydrochloride (Paylean) on welfare indicators for market weight pigs1
Ritter, M. J., Johnson, A. K., Benjamin, M., Carr, S. N., Ellis, M. E., Faucitano, L., Grandin, T., Salak‐Johnson, J. L., Thomson, D. U., Goldhawk, C., et al. (2017) · Translational Animal Science · doi:10.2527/tas2017.0060 · Cited by 14
“Translate basic science to industry innovation of non-essential activities such as feeding, digestion, growth, and reproduction (Sorrells and Sapolsky, 2007; Sorrells et al., 2009).”
Epidermis as the “Third Brain”?
Denda, M. (2015) · Dermatologica Sinica · doi:10.1016/j.dsi.2015.04.011 · Cited by 16
Functional Anatomy and Physiology
Crisler, R., Johnston, N. A., Sivula, C. P., & Budelsky, C. L. (2019) · Elsevier eBooks · doi:10.1016/b978-0-12-814338-4.00004-0 · Cited by 13
Gano, A., Lebonville, C. L., & Becker, H. C. (2022) · The American Journal of Drug and Alcohol Abuse · doi:10.1080/00952990.2022.2092492 · Cited by 13
Thompson, D. J., Weissbecker, I., Cash, E. D., Simpson, D. M., Daup, M., & Sephton, S. E. (2015) · Applied Psychophysiology and Biofeedback · doi:10.1007/s10484-015-9270-4 · Cited by 13
Niemegeers, P., de Boer, P., Schuermans, J., Dumont, G. J. H., Coppens, V., Spittaels, K., Claes, S., Sabbe, B. G. C., & Morrens, M. (2019) · Journal of Affective Disorders · doi:10.1016/j.jad.2018.11.020 · Cited by 12
Steroid-Induced Sleep Disturbance and Delirium: A Focused Review for Critically Ill Patients
Cole, J. L. (2020) · Federal Practitioner · doi:10.12788/fp.0003 · Cited by 12
Komoltsev, I. G., Shalneva, D., Kostyunina, O., Volkova, A. A., Frankevich, S. O., Shirobokova, N. I., Belikova, A., Balan, S. I., Chizhova, O., Salyp, O., et al. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24054542 · Cited by 12
Melief, J., Koper, J. W., Endert, E., Møller, H. J., Hamann, J., Uitdehaag, B. M. J., & Huitinga, I. (2016) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2016.08.019 · Cited by 12
“Moreover,while GChormones are generally considered as anti-inflammatory, there is evidence that they can also have marked pro-inflammatory effects in the brain, in particular on myeloid cells (Sorrells et al., 2009; Sorrells and Sapolsky, 2010).”
Seasonal Variation in Stress Responses∗
Borniger, J. C., Cissé, Y. M., Nelson, R. J., & Martin, L. B. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-802175-0.00041-3 · Cited by 12
Cassiers, L., Niemegeers, P., Fransén, E., Morrens, M., Boer, P. D., Nueten, L. V., Claes, S. J., Sabbe, B., & Eede, F. V. D. (2019) · Brain Sciences · doi:10.3390/brainsci9120375 · Cited by 12
“[53], who reported that chronic stress can induce a reduced cellular immune response to inflammatory stressors.”
BackgroundFudulu, D. P., Horn, G., Hazell, G., Lefrançois-Martinez, A.-M., Martinez, A., Angelini, G. D., Lightman, S. L., & Spiga, F. (2021) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2021.111195 · Cited by 11
Effects of Current Psychotropic Drugs on Inflammation and Immune System
Bhatt, S., Dhar, A. K., Samanta, M. K., & Suttee, A. (2023) · Advances in experimental medicine and biology · doi:10.1007/978-981-19-7376-5_18 · Cited by 12
The link between traumatic stress and autoimmune rheumatic diseases: A systematic scoping review
Ploesser, M., Silverman, S. S., Diaz, J. D. L., Zincke, M. T., & Taylor, M. B. (2024) · Seminars in Arthritis and Rheumatism · doi:10.1016/j.semarthrit.2024.152558 · Cited by 14
The neuroimmune mechanism of pain induced depression in psoriatic arthritis and future directions
Wang, X., Wu, L., Liu, J., Ma, C., Liu, J., & Zhang, Q. (2024) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2024.117802 · Cited by 12
Puga, D. A., Tovar, C. A., Guan, Z., Gensel, J. C., Lyman, M. S., McTigue, D. M., & Popovich, P. G. (2015) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2015.06.006 · Cited by 11
Sheffler, J., Moxley, J. H., & Sachs‐Ericsson, N. (2014) · Aging & Mental Health · doi:10.1080/13607863.2014.880403 · Cited by 11
McEwen, B. S. (2018) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2018.09.011 · Cited by 10
Wagner, A. K., Franzese, K., Weppner, J. L., Kwasnica, C. M., Galang, G., Edinger, J. M., & Linsenmeyer, M. A. (2020) · Elsevier eBooks · doi:10.1016/b978-0-323-62539-5.00043-6 · Cited by 12
Emotional Traumatic Brain Injury
Shulman, L. M. (2020) · Cognitive and Behavioral Neurology · doi:10.1097/wnn.0000000000000243 · Cited by 9
Sun, L., Saliba, S. W., Apweiler, M., Akmermer, K., Herlan, C., Grathwol, C. W., de Oliveira, A. C. P., Normann, C., Jung, N., Bräse, S., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25084462 · Cited by 9
“Previous studies have reported that the experimental activation of microglia exacerbated the development of depressive-like behaviors in animal models [57] and antidepressant drugs were shown to alleviate the activation of microglia [58,59].”
ResultHippocampus under Pressure: Molecular Mechanisms of Development of Cognitive Impairments in SHR Rats
Stepanichev, M. Y., Mamedova, D. I., & Gulyaeva, N. V. (2024) · Biochemistry (Moscow) · doi:10.1134/s0006297924040102 · Cited by 9
Kumari, R., Verma, V., & Singaravel, M. (2024) · Neuroscience · doi:10.1016/j.neuroscience.2024.01.026 · Cited by 9
Ord, J., Fazeli, A., & Watt, P. J. (2017) · Advances in experimental medicine and biology · doi:10.1007/978-3-319-62414-3_7 · Cited by 9
Immune-Endocrine Links to Gregariousness in Wild House Mice
Lopes, P. C., Carlitz, E. H. D., Kindel, M., & König, B. (2020) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2020.00010 · Cited by 9
Bertin, J. O., Dury, A. Y., Ke, Y., Ouellet, J., & Labrie, F. (2015) · Steroids · doi:10.1016/j.steroids.2015.02.013 · Cited by 9
Usage of corticosteroids as therapeutic agents in diseases
Al‐Mosawi, R. H., & Alebadi, N.-A. M. (2023) · Medical Journal of Babylon · doi:10.4103/mjbl.mjbl_391_23 · Cited by 8
Coffee and mental disorders: How caffeine affects anxiety and depression
Meamar, M., Raise‐Abdullahi, P., Rashidy‐Pour, A., & Raeis-Abdollahi, E. (2024) · Progress in brain research · doi:10.1016/bs.pbr.2024.06.015 · Cited by 13
Microbiome‐gut‐brain axis as a novel hotspot in depression
Ma, Y., Xu, P., Bai, Z., & Fang, J. (2024) · Brain‐X · doi:10.1002/brx2.43 · Cited by 9
Colgan, D. D., Eddy, A., Bowen, S. W., & Christopher, M. (2019) · Journal of Police and Criminal Psychology · doi:10.1007/s11896-019-09336-3 · Cited by 8
Is SARS-CoV-2 a Risk Factor of Bipolar Disorder?—A Narrative Review
Lorkiewicz, P., & Waszkiewicz, N. (2022) · Journal of Clinical Medicine · doi:10.3390/jcm11206060 · Cited by 8
Perveen, T., Emad, S., Haider, S., Sadaf, S., Qadeer, S., Batool, Z., Sarfaraz, Y., & Sheikh, S. (2017) · Neuroscience · doi:10.1016/j.neuroscience.2017.11.014 · Cited by 8
MacDowell, K. S., Martín‐Hernández, D., Ulecia-Morón, C., Bris, Á. G., Madrigal, J. L. M., García‐Bueno, B., & Caso, J. R. (2020) · International Immunopharmacology · doi:10.1016/j.intimp.2020.107217 · Cited by 8
Self-citationWoodruff, R. T., Schorpp, K., Lawrenczyk, A. J., Chakraborty, T., & Kusnecov, A. W. (2010) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2010.10.005 · Cited by 8
Hasan, Z. W., Nguyen, V. T., & Ashley, N. T. (2024) · PeerJ · doi:10.7717/peerj.17539 · Cited by 7
“While GCs are well-known for their anti-inflammatory properties, in acute stress conditions, they can have a ‘‘priming’’ effect, shifting GCs towards pro-inflammatory effects ( Sorrells et al., 2009 ).”
BackgroundThe stress-immune system axis: Exploring the interplay between stress and immunity
Raza, M. L. (2025) · Progress in brain research · doi:10.1016/bs.pbr.2025.01.003 · Cited by 8
Therapeutic effects of exercise on depression: The role of microglia
Li, L., Ren, L., Ren, L., & Li, B. (2024) · Brain Research · doi:10.1016/j.brainres.2024.149279 · Cited by 7
Cheng, J., Zhang, J., Lu, C., & Wang, L. (2012) · Neuroscience Bulletin · doi:10.1007/s12264-012-1246-2 · Cited by 7
Onishi-Kato, Y., Nakamura, M., Iwanami, A., Kato, M., Suzuki, T., Kosugi, S., Katori, N., Hashiguchi, S., Tsuzaki, K., Takeda, J., et al. (2017) · Clinical Journal of Pain · doi:10.1097/ajp.0000000000000438 · Cited by 7
Martínez, A. D., Mercado, E., Barbieri, M., Kim, S. Y., & Granger, D. A. (2022) · Frontiers in Public Health · doi:10.3389/fpubh.2021.762735 · Cited by 8
Maikoo, S., Wilkins, A., & Qulu, L. (2022) · IBRO Neuroscience Reports · doi:10.1016/j.ibneur.2022.05.001 · Cited by 6
Szteroidok: A glükokortikoidok élettani és gyógyszertani hatásai
Zelena, D., & Makara, B. G. (2015) · Orvosi Hetilap · doi:10.1556/650.2015.30248 · Cited by 6
Foley, T. D., Koval, K. S., Gallagher, A. G., & Olsen, S. H. (2018) · Metabolic Brain Disease · doi:10.1007/s11011-018-0340-1 · Cited by 6
Brymer, K. J., Kulhaway, E. Y., Howland, J. G., Caruncho, H. J., & Kalynchuk, L. E. (2021) · Behavioural Brain Research · doi:10.1016/j.bbr.2021.113291 · Cited by 6
Cheng, X., Cai, X., Ma, J., Feng, Y., Zou, Z., Wang, W., Chen, L., & Yao, B. (2025) · Clinical and Experimental Nephrology · doi:10.1007/s10157-025-02732-6 · Cited by 5
Salimiyan, S., Mohammadi, M., Akbari, S. A., Kazemi, R., Amini, A. A., & Rahmani, M. R. (2022) · Journal of Interferon & Cytokine Research · doi:10.1089/jir.2021.0120 · Cited by 5
Voituron, Y., Roussel, D., Galliard, J. L., Dupoué, A., Romestaing, C., & Meylan, S. (2022) · Journal of Comparative Physiology B · doi:10.1007/s00360-022-01454-5 · Cited by 5
Sabei, L., Sarmiento, M. P., Bernardino, T., Çakmakçı, C., Farias, S. D. S., Sato, D., Zanella, M. I. G., Poletto, R., & Zanella, A. J. (2023) · Frontiers in Animal Science · doi:10.3389/fanim.2023.1208768 · Cited by 5
Gilstrap, S. R., Hobson, J. M., Owens, M. A., White, D. M., Sammy, M. J., Ballinger, S. W., Sorge, R. E., & Goodin, B. R. (2023) · Molecular Pain · doi:10.1177/17448069231195975 · Cited by 16
FKBP5 mediates glucocorticoid signaling in estrogen deficiency-associated endothelial dysfunction
Zhu, R., Xu, Y., Li, H., He, C., Leung, F. P., Wang, L., & Wong, W. T. (2025) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2025.177598 · Cited by 5
Paakinaho, V., Kaikkonen, S., Levonen, A., & Palvimo, J. J. (2014) · Molecular and Cellular Biology · doi:10.1128/mcb.00748-14 · Cited by 5
“However, in prolonged stress, the effects of glucocorticoids can become proinflammatory (8, 9).”
BackgroundThe Inflammatory Hypothesis of Depression
Soskin, D. P., Cassiello-Robbins, C. F., Isacoff, O. K., & D, M. F. M. (2012) · FOCUS The Journal of Lifelong Learning in Psychiatry · doi:10.1176/appi.focus.10.4.413 · Cited by 5
Neuroimmune Response Mediated by Cytokines in Natural Scrapie after Chronic Dexamethasone Treatment
Guijarro, I. M., Garcés, M., Andrés‐Benito, P., Marín, B., Otero, A., Barrio, T., Carmona, M., Ferrer, I., Badiola, J. J., & Monzón, M. (2021) · Biomolecules · doi:10.3390/biom11020204 · Cited by 5
“In most cases, chronic exposition to GC suppresses mediators; however, on some occasions, GC can potentiate such immunity [47], especially in the central nervous system, which can exacerbate neuronal death [48].”
BackgroundNeuroimmune Response in Natural Preclinical Scrapie after Dexamethasone Treatment
Guijarro, I. M., Garcés, M., Marín, B., Otero, A., Barrio, T., Badiola, J. J., & Monzón, M. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21165779 · Cited by 5
“This is based on the fact that the mechanisms underlying cytokine release could be a crucial target for therapeutic approaches in the central nervous system (CNS) in prion diseases [25].”
BackgroundMicroglia and Systemic Immunity
Jucá, P. M., Duque, É. D. A., Covre, L. H. H., Albernaz-Mariano, K. A., & Munhoz, C. D. (2024) · Advances in neurobiology · doi:10.1007/978-3-031-55529-9_16 · Cited by 6
Self-citationInflammatory Biomarkers and Neurotransmitter Perturbations in Delirium
Maldonado, J. R. (2020) · Springer eBooks · doi:10.1007/978-3-030-25751-4_10 · Cited by 6
Kristóf, Z., Szabó, D., Sperlágh, B., Török, D., & Gonda, X. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26104687 · Cited by 5
“Upon acute stress, the HPA system releases glucocorticoids that stimulate both the well-known anti-and lesser-known pro-inflammatory responses [98,99] (Figure 1).”
Qin, S., Yang, J., Wang, Z., He, P., Dong, T., Ren, Z., & Li, Q. (2025) · Frontiers in Medicine · doi:10.3389/fmed.2025.1605931 · Cited by 4
Mueller, B. R. (2023) · Current Pain and Headache Reports · doi:10.1007/s11916-023-01173-8 · Cited by 4
“Stress is recognized as an important risk factor for both POTS and migraine, and there is accumulating evidence that dysregulation of stress response systems is common to both conditions [7, 8].”
BackgroundLion, M., Muller, M., Ibrahim, E. C., El‐Hage, W., Lengvenytė, A., Courtet, P., Antoine Lefrere, A., & Belzeaux-R, R. (2024) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2024.111227 · Cited by 4
Denda, M. (2016) · Springer eBooks · doi:10.1007/978-3-319-43157-4_19 · Cited by 4
Alekseeva, L. A., Bessonova, T. V., Makarenkova, E. V., Zhirkov, A., Monakhova, N. E., Vilnits, A., & Gorelik, E. (2020) · Pediatrician (St Petersburg) · doi:10.17816/ped11421-28 · Cited by 2
“Кортизол обладает выраженным противовоспалительным действием, способен снижать проницаемость капилляров, угнетать процессы клеточного деления и биосинтез белка, стабилизировать мембраны лизосом, воздействовать на иммунные реакции, в частности синтез цитокинов, функциональную активность иммунокомпетентных клеток, непос…”
Tsaousi, G. G., Pourzitaki, C., Kapanidis, K., Mavrantoni, E., Καπουκρανίδου, Δ., & Kouvelas, D. (2021) · Behavioural Brain Research · doi:10.1016/j.bbr.2021.113728 · Cited by 4
Caso, J. R., MacDowell, K. S., Soto, M., Ruiz-Guerrero, F., Carrasco-Díaz, Á., Leza, J. C., Carrasco, J. L., & Díaz‐Marsá, M. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.846172 · Cited by 5
“Glucocorticoids participate in the modulation of inflammatory processes and an elevation of their levels could translate into a dysregulation of the immune response (Sorrells et al., 2009).”
BackgroundSelf-citationWerdani, Y. D. W. (2022) · Public Health and Preventive Medicine Archive · doi:10.53638/phpma.2020.v8.i1.p09 · Cited by 4
Pukhalsky, A. L., Шмарина, Г. В., & Aleshkin, V. A. (2014) · Annals of the Russian academy of medical sciences · doi:10.15690/vramn.v69i5-6.1038 · Cited by 4
Ketamine for atypical facial pain and hormonal dysregulation: a case report
Darwish, Y., Willeford, S., Mahesh, K., & Van, S. (2023) · Regional Anesthesia & Pain Medicine · doi:10.1136/rapm-2023-104482 · Cited by 4
Mazlan, M. (2017) · Elsevier eBooks · doi:10.1016/b978-0-323-47904-2.00043-x · Cited by 4
Glannon, W. (2018) · Oxford University Press eBooks · doi:10.1093/med/9780198758853.003.0009 · Cited by 4
Petruso, F., Giff, A. E., Milano, B. A., Rossi, M. M. D., & Saccaro, L. F. (2023) · doi:10.31234/osf.io/2rnk8 · Cited by 4
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
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.
A language model drew the claims from the paper on 2026-10-11, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-11 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
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 ›
Are you an author, or do you see a problem with this page? Request a review
