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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“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).”
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“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]
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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
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Sorted by citations
Items 101–200 of 426
The neuroendocrine control of the innate immune system in health and brain diseases
Bellavance, M., & Rivest, S. (2012) · Immunological Reviews · doi:10.1111/j.1600-065x.2012.01129.x · Cited by 61
“In addition, the length of exposure, route of administration, and type of synthetic GR agonists employed have also been recognized as important determinants (133).”
BackgroundAlameda, L., Fournier, M., Khadimallah, I., Griffa, A., Cleusix, M., Jenni, R., Ferrari, C., Klauser, P., Baumann, P., Cuénod, M., et al. (2018) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1812821115 · Cited by 61
“However, this regulation is impaired if stress exposure persists for months, as shown by human and primate studies reporting alterations of HPA axis activation in children exposed to severe life stress (31), and glucocorticoids induced by acute stress may actually prime neuroinflammation to subsequent challenges (32,…”
Neuroimmune and Inflammatory Signals in Complex Disorders of the Central Nervous System
Liberman, A. C., Trías, E., Chagas, L. D. S., Trindade, P., Pereira, M. D. S., Refojo, D., Hedin‐Pereira, C., & Serfaty, C. A. (2018) · NeuroImmunoModulation · doi:10.1159/000494761 · Cited by 62
Breaking Boundaries in Neural-Immune Interactions
McAllister, A. K., & de Water, J. V. (2009) · Neuron · doi:10.1016/j.neuron.2009.09.038 · Cited by 59
“Increased levels of proinflammatory cytokines and neural inflammation, stimulated by chronic stress (see Sorrells et al., 2009 [this issue of Neuron]), likely also contribute to the altered synaptic plasticity and long-term cognitive changes in depression.”
BackgroundTrait anxiety reduces affective fading for both positive and negative autobiographical memories
Walker, W. R., & Yancu, C. N. (2014) · Advances in Cognitive Psychology · doi:10.5709/acp-0159-0 · Cited by 61
Factors promoting vulnerability to dysregulated stress reactivity and stress‐related disease
Russell, A. L., Tasker, J. G., Lucion, A. B., Fiedler, J. L., Munhoz, C. D., Wu, T. J., & Deak, T. (2018) · Journal of Neuroendocrinology · doi:10.1111/jne.12641 · Cited by 66
Self-citationPedrazzoli, M., Losurdo, M., Paolone, G., Medelin, M., Jaupaj, L., Cisterna, B., Slanzi, A., Malatesta, M., Coco, S., & Buffelli, M. (2019) · Neurobiology of Disease · doi:10.1016/j.nbd.2019.104568 · Cited by 58
Kim, S., Park, E. S., Chen, P. R., & Kim, E. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.864858 · Cited by 61
Santarsieri, M., Kumar, R. G., Kochanek, P. M., Berga, S. L., & Wagner, A. K. (2014) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2014.09.003 · Cited by 62
Oxidative stress: a potential link between emotional wellbeing and immune response
Salim, S. (2016) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2016.06.006 · Cited by 68
Glial and tissue-specific regulation of Kynurenine Pathway dioxygenases by acute stress of mice
Dostal, C. R., Sulzer, M. C., Kelley, K. W., Freund, G. G., & McCusker, R. H. (2017) · Neurobiology of Stress · doi:10.1016/j.ynstr.2017.02.002 · Cited by 58
“Stress is associated with immunological changes both in the periphery and CNS (Frank et al., 2015; Sorrells et al., 2009).”
BackgroundInfluentialLoram, L. C., Taylor, F. R., Strand, K. A., Frank, M. G., Sholar, P. W., Harrison, J. A., Maier, S. F., & Watkins, L. R. (2011) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2011.04.013 · Cited by 57
“During periods of stress, glucocorticoids are not the only hormones released that influence immune function (Sorrells et al., 2009).”
BackgroundInfluentialHorowitz, M. A., Cattaneo, A., Cattane, N., Lopizzo, N., Tojo, L. M., Bakunina, N., Musaelyan, K., Borsini, A., Zunszain, P. A., & Pariante, C. M. (2020) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2020.03.012 · Cited by 61
“A second hypothesis focuses on recent evidence that cortisol possesses more complex immunomodulatory effects than have previously been ascribed to it: in particular, that under certain circumstances, glucocorticoids can be potentiate inflammatory processes, in addition to its recognized inhibitory effects (Cain and Ci…”
BackgroundArnaldo, I., Corcoran, A. W., Friston, K. J., & Ramstead, M. J. D. (2022) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2022.104590 · Cited by 56
“Intermediate activation of GR receptors is necessary for memory consolidation, but saturation of GRs results in memory impairments (Finsterwald and Alberini, 2014; Peters et al., 2017; Sorrells et al., 2009).”
Lerch, J. K., Puga, D. A., Bloom, O., & Popovich, P. G. (2014) · Seminars in Immunology · doi:10.1016/j.smim.2014.03.004 · Cited by 56
Child Poverty and the Promise of Human Capacity: Childhood as a Foundation for Healthy Aging
Wise, P. H. (2016) · Academic Pediatrics · doi:10.1016/j.acap.2016.01.014 · Cited by 63
Markovic, V. M., Cupic, Z., Vukojevic, V., & Kolar-Anic, L. (2011) · Endocrine Journal · doi:10.1507/endocrj.ej11-0037 · Cited by 54
Zannas, A. S., McQuoid, D. R., Payne, M. E., Steffens, D. C., MacFall, J. R., Ashley-Koch, A., & Taylor, W. D. (2013) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2013.02.008 · Cited by 53
“The neurotoxicity hypothesis posits that chronic hyperactivity of the stress system in MDD leads to decreased neurogenesis, augmented neuroinflammation, dendritic retraction, and accelerated apoptosis (Lucassen et al., 2006; Sorrells et al., 2009).”
BackgroundNoradrenaline as a key neurotransmitter in modulating microglial activation in stress response
Sugama, S., & Kakinuma, Y. (2020) · Neurochemistry International · doi:10.1016/j.neuint.2020.104943 · Cited by 63
Kemp, G. M., Altimimi, H. F., Nho, Y., Heir, R., Klyczek, A., & Stellwagen, D. (2022) · Molecular Psychiatry · doi:10.1038/s41380-022-01737-x · Cited by 59
The Involvement of Neuroinflammation in the Onset and Progression of Parkinson’s Disease
Jurcău, A., Andronie-Cioară, F. L., Nistor-Cseppento, C. D., Pașcalău, N., Rus, M., Vasca, E., & Jurcău, M. C. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241914582 · Cited by 58
“However, studies performed on both the peripheral and central nervous system showed that under specific conditions relating to the timing and duration of stress, glucocorticoids may promote CNS inflammation and activate microglia toward the M1 phenotype [264].”
Corticosteroids limit microglial activation occurring during acute stress
Sugama, S., Takenouchi, T., Fujita, M., Kitani, H., Conti, B., & Hashimoto, M. (2012) · Neuroscience · doi:10.1016/j.neuroscience.2012.12.012 · Cited by 54
“This, together with the finding that higher doses of glucocorticoids potentiated the expression of pro-inflammatory cytokines in cultured neurons (MacPherson et al., 2005), suggested that glucocorticoids may have a pro-inflammatory role (Sorrells et al., 2009).”
BackgroundBrás, J. P., de Suduiraut, I. G., Zanoletti, O., Monari, S., Meijer, M., Grosse, J., Barbosa, M. A., Santos, S. G., Sandi, C., & Almeida, M. I. (2021) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2021.10.018 · Cited by 58
IFN-γ differentially modulates memory-related processes under basal and chronic stressor conditions
Litteljohn, D., Nelson, E., & Hayley, S. P. (2014) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2014.00391 · Cited by 53
Maturana, C. J., Aguirre, A., & Sáez, J. C. (2016) · Developmental Neurobiology · doi:10.1002/dneu.22409 · Cited by 51
“Secretion of GCs from the adrenal cortex is controlled by the hypothalamic– pituitary–adrenal (HPA) axis, which is activated by a stressor and is part of a response that allows the organism to adapt to changes in the environment (Sorrells et al., 2009; Popoli et al., 2012).”
BackgroundInfluentialKelly, K. A., Michalovicz, L. T., Miller, J. V., Castranova, V., Miller, D. B., & O'Callaghan, J. P. (2018) · PLoS ONE · doi:10.1371/journal.pone.0190546 · Cited by 54
Diabetes type II: A risk factor for depression-Parkinson–Alzheimer?
Riederer, P., Bartl, J., Laux, G., & Grünblatt, E. (2011) · Neurotoxicity Research · doi:10.1007/s12640-010-9203-1 · Cited by 51
“It was shown that especially depression occurs in 25–50% of PD patients (Bodis-Wollner 2003; Berg 2008): maladaptation to long-term stress may dysregulate the HPA axis (Checkley 1996; Dinan 2005; Sorrells et al. 2009) thus contributing to the pathogenesis of parkinson-”
BackgroundGriffin, G. D., Charron, D. J., & Al‐Daccak, R. (2014) · Clinical & Translational Immunology · doi:10.1038/cti.2014.26 · Cited by 50
Kennard, J. A., & Woodruff‐Pak, D. S. (2012) · Physiology & Behavior · doi:10.1016/j.physbeh.2012.02.023 · Cited by 52
“Another potential explanation involves priming of the stress and inflammatory response systems [34].”
BackgroundEffects of trauma, economic hardship, and stress on neurocognition and everyday function in HIV.
Watson, C. W., Sundermann, E. E., Hussain, M., Umlauf, A., Thames, A. D., Moore, R. C., Letendre, S. L., Jeste, D. V., Morgan, E. E., & Moore, D. J. (2018) · Health Psychology · doi:10.1037/hea0000688 · Cited by 51
Nuclear deterrents: Intrinsic regulators of IL-1β-induced effects on hippocampal neurogenesis
Ó’Léime, C. S., Cryan, J. F., & Nolan, Y. M. (2017) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2017.07.153 · Cited by 53
Dim Light at Night Increases Immune Function in Nile Grass Rats, a Diurnal Rodent
Fonken, L. K., Haim, A., & Nelson, R. J. (2012) · Chronobiology International · doi:10.3109/07420528.2011.635831 · Cited by 49
“The role of glucocorticoids in immunological processes are complex, however (Sorrells et al., 2009); depending on the type of stress, glucocorticoids can have opposite effects.”
BackgroundDegaspari, S., Tzanno-Martins, C., Fujihara, C. K., Zatz, R., Branco-Martins, J. P., Viel, T. A., Buck, H. S., Orellana, A. M., Böhmer, A. E., Lima, L. D. S., et al. (2015) · PLoS ONE · doi:10.1371/journal.pone.0125271 · Cited by 47
“However, there are circumstances following an inflammatory challenge or insult where GCs or stress enhance rather than blunt inflammation [54].”
BackgroundSelf-citationThe Immune System in Stroke: Clinical Challenges and Their Translation to Experimental Research
Smith, C. J., Lawrence, C. B., Rodriguez‐Grande, B., Kovács, K., Pradillo, J. M., & Dénes, Á. (2013) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-013-9469-1 · Cited by 47
“immune response (acute effect), brief glucocorticoid exposure enhances immune responses to subsequent inflammatory insults (priming effect) and chronic exposure to very high steroid doses are immunosuppressive (Sorrells and Sapolsky 2007; Sorrells et al. 2009).”
BackgroundThe permissive role of glucocorticoids in neuroinflammatory priming
Frank, M. G., Watkins, L. R., & Maier, S. F. (2015) · Current Opinion in Endocrinology Diabetes and Obesity · doi:10.1097/med.0000000000000168 · Cited by 48
“However, mounting evidence now suggests that glucocorticoids, in some contexts, may promote or potentiate inflammatory immune responses [3], findings that have prompted a re-evaluation of the dogma that glucocorticoids are universally anti-inflammatory.”
BackgroundGlucocorticoid signaling in myeloid cells worsens acute CNS injury and inflammation
Sorrells, S. F., Caso, J. R., Munhoz, C. D., Hu, C. K., Tran, K. V., Miguel, Z. D., Chien, B. Y., & Sapolsky, R. M. (2013) · The Journal of Neuroscience · doi:10.1523/jneurosci.4705-12.2013 · Cited by 46
“, 2010); however, recent evidence suggests that GCs do not always decrease inflammation and, depending on the context of their exposure, may even increase inflammatory responses (for review, see Dhabhar, 2009; Sorrells et al., 2009).”
Petruso, F., Giff, A., Milano, B. A., Rossi, M. M. D., & Saccaro, L. F. (2023) · Neuronal Signaling · doi:10.1042/ns20220077 · Cited by 53
“We have gathered direct and indirect evidence from several studies about inflammation in BPD. Multiple groups have demonstrated associations among salivary hypocortisolism, inflammatory cytokines, and stress-related chronic pain [380,381].”
BackgroundAdhya, D., Annuario, E., Lancaster, M. A., Price, J., Baron‐Cohen, S., & Srivastava, D. P. (2017) · Journal of Neuroendocrinology · doi:10.1111/jne.12547 · Cited by 45
Brain Trauma, Glucocorticoids and Neuroinflammation: Dangerous Liaisons for the Hippocampus
Komoltsev, I. G., & Gulyaeva, N. V. (2022) · Biomedicines · doi:10.3390/biomedicines10051139 · Cited by 43
“The effects of GCs are critically determined by the specific aspects of their action [70].”
BackgroundPost-traumatic Stress Disorder: Focus on Neuroinflammation
Li, J., Tong, L., Schock, B. C., & Ji, L.-L. (2023) · Molecular Neurobiology · doi:10.1007/s12035-023-03320-z · Cited by 47
Martín‐Montañez, E., Pavía, J., Santín, L. J., Boraldi, F., Estivill‐Torrús, G., Aguirre, J. A., & Garcia‐Fernandez, M. I. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2014.03.010 · Cited by 44
“The presence of the antioxidant effect of IGF-II could explain responses of nervous system tissue to IGF-II under oxidative damage, in which an increase in the levels of IGF-II were detected under pathologic conditions, such as ischemia, hypoxia [52,75], amyotrophic lateral sclerosis [76,77] and traumatic brain injury…”
BackgroundRelevance of chronic stress and the two faces of microglia in Parkinson's disease
Herrera, A. J., Espinosa-Oliva, A. M., Carrillo-Jiménez, A., Oliva-Martín, M. J., García-Revilla, J., García-Quintanilla, A., de Pablos, R. M., & Venero, J. L. (2015) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2015.00312 · Cited by 42
“However, as mentioned earlier in this review, the timing and duration of stress responsemay be critical formodulating the immune response (Sorrells et al., 2009).”
BackgroundDysfunction of inflammatory pathways in adolescent female patients with anorexia nervosa
Caso, J. R., Graell, M., Navalón, A., MacDowell, K. S., Gutiérrez, S., Soto, M., Leza, J. C., Carrasco, J. L., & Díaz‐Marsá, M. (2019) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2019.109727 · Cited by 43
Self-citationWillette, A. A., Coe, C. L., Colman, R. J., Bendlin, B. B., Kastman, E. K., Field, A. S., Alexander, A. L., Allison, D. B., Weindruch, R. H., & Johnson, S. C. (2012) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2011.10.006 · Cited by 41
“Biological mediators of this CR effect may include lower stress-induced cortisol release (Sorrells et al., 2009), or alterations in energy and oxidative metabolism that occur in part by increasing orexin signaling and decreasing markers of cellular aging (Inoue et al.”
BackgroundMissing and Possible Link between Neuroendocrine Factors, Neuropsychiatric Disorders, and Microglia
Kato, T. A., Hayakawa, K., Monji, A., & Kanba, S. (2013) · Frontiers in Integrative Neuroscience · doi:10.3389/fnint.2013.00053 · Cited by 43
“Minocycline has a variety of functions in the CNS such as interacting with brain glutamate and dopamine neurotransmission (Kim and Suh, 2009) and having direct effects on neuronal cells (Hashimoto and Ishima, 2010).”
BackgroundInfluentialThe Role of Steroid Hormones in the Modulation of Neuroinflammation by Dietary Interventions
Vasconcelos, A. R., Cabral‐Costa, J. V., Mazucanti, C. H., Scavone, C., & Kawamoto, E. M. (2016) · Frontiers in Endocrinology · doi:10.3389/fendo.2016.00009 · Cited by 41
Westfall, S., Iqbal, U. H., Sebastian-Valverde, M., & Pasinetti, G. M. (2019) · Progress in molecular biology and translational science · doi:10.1016/bs.pmbts.2019.06.013 · Cited by 42
Is there a role for the nuclear receptor PPARγ in neuropsychiatric diseases?
García‐Bueno, B., Perez‐Nievas, B. G., & Leza, J. C. (2010) · The International Journal of Neuropsychopharmacology · doi:10.1017/s1461145710000970 · Cited by 41
“However, in recent years the classic view that GCs are universally anti-inflammatory has been challenged at a variety of levels, including the CNS (Sorrells et al. 2009).”
BackgroundNguyen, D. N., Huyghens, L., Zhang, H., Schiettecatte, J., Smitz, J. E. J., & Vincent, J. (2014) · BioMed Research International · doi:10.1155/2014/712742 · Cited by 40
“In addition, the BBB breakdown in sepsis could worsen brain dysfunction by facilitating a crossing of cortisol, toxic amino acids and other proinflammatorymediators from the blood into the brain [25–27].”
BackgroundMechanistic insights into corticosteroids in multiple sclerosis: War horse or chameleon?☆
Krieger, S. C., Sorrells, S. F., Nickerson, M., & Pace, T. W. W. (2014) · Clinical Neurology and Neurosurgery · doi:10.1016/j.clineuro.2013.12.021 · Cited by 40
Self-citationNeuroimmunology of status epilepticus
Vezzani, A., Sapia, R. D., Kebede, V., Balosso, S., & Ravizza, T. (2023) · Epilepsy & Behavior · doi:10.1016/j.yebeh.2023.109095 · Cited by 39
Glucocorticoid programming of neuroimmune function
Walker, D. J., & Spencer, K. A. (2017) · General and Comparative Endocrinology · doi:10.1016/j.ygcen.2017.07.016 · Cited by 42
“GR is ubiquitously expressed throughout the CNS with high levels of expression in neurons and microglia (Sorrells et al., 2009), while MR expression is confined to a few regions, such as the hippocampus, amygdala and neurons within the PVN of the hypothalamus (Reul and de Kloet,”
BackgroundInfluentialGlucocorticoids, metabolism and brain activity
Jaszczyk, A., & Juszczak, G. R. (2021) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2021.03.007 · Cited by 45
Physiological and behavioural responsivity to stress and anxiogenic stimuli in COMT-deficient mice
Desbonnet, L., Tighe, O., Karayiorgou, M., Gogos, J. A., Waddington, J. L., & O’Tuathaigh, C. M. P. (2012) · Behavioural Brain Research · doi:10.1016/j.bbr.2011.12.014 · Cited by 38
Murta, V., & Ferrari, C. C. (2012) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2012.06.004 · Cited by 38
“Indeed, recent data demonstrated that glucocorticoids (GCs), considered as potent anti-inflammatory molecules, under certain circumstances can exert pro-inflammatory effects (reviewed in (Sorrells et al., 2009)).”
Mkhize, N. V., Qulu, L., & Mabandla, M. V. (2017) · Journal of Experimental Neuroscience · doi:10.1177/1179069517704668 · Cited by 40
Yoshiya, M., Komatsuzaki, Y., Hojo, Y., Ikeda, M., Mukai, H., Hatanaka, Y., Murakami, G., Kawata, M., Kimoto, T., & Kawato, S. (2013) · Frontiers in Neural Circuits · doi:10.3389/fncir.2013.00191 · Cited by 38
“The application of CORT at 100, 500, and 1000 nM induced a rapid increase in the density of thorns in the stratum lucidum of CA3 pyramidal neurons.”
BackgroundGan, Y., Wang, C., He, R.-H., Hsu, P.-C., Yeh, H.-H., Hsieh, T.-H., Lin, H., Cheng, M.-Y., Jeng, C., Huang, M., et al. (2022) · Journal of Neuroinflammation · doi:10.1186/s12974-022-02517-8 · Cited by 40
“As to the important finding on the TNF-α levels between Fkpb5-KO-CTL and Fkpb5-KO-DEX, it was reported that chronic HPA axis activation would induce neuroinflammation [65, 66].”
BackgroundMyalgic Encephalomyelitis: Symptoms and Biomarkers
Jason, L. A., Zinn, M. L., & Zinn, M. A. (2015) · Current Neuropharmacology · doi:10.2174/1570159x13666150928105725 · Cited by 38
“Contrary to the aforementioned functional imaging evidence showing CNS hypofunction, Wyller, Eriksen, and Malterud [171] hypothesize that sustained arousal is the primary mechanism of ME.”
BackgroundInfluentialCorticosteroids, but not NSAIDs, are associated with less Alzheimer neuropathology
Beeri, M. S., Schmeidler, J., Lesser, G. T., Maroukian, M., West, R. K., Leung, S., Wysocki, M., Perl, D. P., Purohit, D. P., & Haroutunian, V. H. (2011) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2011.02.011 · Cited by 36
PTSD, Immune System, and Inflammation
Pivac, N., Vuić, B., Šagud, M., Erjavec, G. N., Perković, M. N., Konjevod, M., Tudor, L., Štrac, D. Š., Uzun, S., Kozumplik, O., et al. (2023) · Advances in experimental medicine and biology · doi:10.1007/978-981-19-7376-5_11 · Cited by 38
Gupta, A., Labus, J. S., Kilpatrick, L. A., Bonyadi, M., Ashe-McNalley, C., Heendeniya, N., Bradesi, S., Chang, L., & Mayer, E. A. (2015) · Brain Structure and Function · doi:10.1007/s00429-015-0996-9 · Cited by 36
“While GC receptor activation typically downregulates inflammatory gene expression, chronic psychosocial stress can result in desensitization of GCR proteins and a failure of GCs to regulate GCR response genes, even in the presence of normal or elevated GC levels (Sorrells et al. 2009; Slavich and Cole 2013).”
Wincewicz, D., Juchniewicz, A., Waszkiewicz, N., & Braszko, J. J. (2016) · Pharmacology Biochemistry and Behavior · doi:10.1016/j.pbb.2016.06.010 · Cited by 34
Komoltsev, I. G., Frankevich, S. O., Shirobokova, N. I., Volkova, A. A., Onufriev, M. V., Moiseeva, J. V., Novikova, M. R., & Gulyaeva, N. V. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22115883 · Cited by 34
“It is suggested that in the hippocampus GCs may act as pro-inflammatory agents [8,53,54].”
BackgroundTakei, K., Denda, S., Kumamoto, J., & Denda, M. (2013) · Experimental Dermatology · doi:10.1111/exd.12224 · Cited by 35
“I Don’t Know Why I’ve Got this Pain!” Allostasis as a Possible Explanatory Model
Rabey, M. I., & Moloney, N. A. (2022) · Physical Therapy · doi:10.1093/ptj/pzac017 · Cited by 32
Sports and Immunity, from the recreational to the elite athlete
Baskerville, R., Castell, L. M., & Bermon, S. (2024) · Infectious Diseases Now · doi:10.1016/j.idnow.2024.104893 · Cited by 40
Wilson, J. B., Epstein, M., Lopez, B., Brown, A. K., Lutfy, K., & Friedman, T. C. (2023) · Frontiers in Endocrinology · doi:10.3389/fendo.2023.1224612 · Cited by 35
The central role of microglia in major depressive disorder and its potential as a therapeutic target
Xia, X., Li, K., Zou, W., & Wang, L. (2025) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2025.1598178 · Cited by 31
Do epidermal keratinocytes have sensory and information processing systems?
Denda, M., & Nakanishi, S. (2021) · Experimental Dermatology · doi:10.1111/exd.14494 · Cited by 31
Incoherent feed-forward regulatory logic underpinning glucocorticoid receptor action
Chen, S., Masuno, K., Cooper, S., & Yamamoto, K. R. (2013) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1216108110 · Cited by 31
dos Santos, N. B., Novaes, L. S., Dragunas, G., Rodrigues, J. R., Brandão, W. N., Camarini, R., Peron, J. P. S., & Munhoz, C. D. (2019) · Scientific Reports · doi:10.1038/s41598-019-43217-3 · Cited by 32
Self-citationFakhri, S., Abbaszadeh, F., & Jorjani, M. (2021) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2021.111563 · Cited by 30
Relationship between energy dense diets and white adipose tissue inflammation in metabolic syndrome
Alemany, M. (2012) · Nutrition Research · doi:10.1016/j.nutres.2012.11.013 · Cited by 28
“[75] Sorrells SF, Caso JR, Munhoz CD, Sapolsky RM.”
BackgroundCytokines and Cytokine Receptors Involved in the Pathogenesis of Alzheimers Disease
Nagae, T., & Araki, K. (2016) · Journal of Clinical & Cellular Immunology · doi:10.4172/2155-9899.1000441 · Cited by 28
“The elevation of glucocorticoids (GCs) secreted by the adrenal glands upon chronically stressful stimuli that occurs during aging may accelerate the progression of brain aging, particularly the hippocampus.”
BackgroundInfluentialA refined blood collection method for quantifying corticosterone
Milot, M. R., James, J. S., Merali, Z., & Plamondon, H. (2012) · Lab Animal · doi:10.1038/laban0312-77 · Cited by 28
“Corticosterone also has a central role in inhibiting activity of the hypothalamic–pituitary–adrenal axis, which mediates the major neuroendocrine responses to stress, and is known to regulate immune response”
BackgroundGastrointestinal microbiota and inflammasomes interplay in health and disease: a gut feeling
Luca, R. D., Arrè, V., Nardone, S., Incerpi, S., Giannelli, G., Trivedi, P., Anastasiadou, E., & Negro, R. (2025) · Gut · doi:10.1136/gutjnl-2025-334938 · Cited by 33
“138 The gut microbiota regulates the HPA axis and mediates the interaction between stress and inflammation.”
Stress and Glucose metabolism: A Review
Yajurvedi, H. N. (2018) · Imaging Journal of Clinical and Medical Sciences · doi:10.17352/2455-8702.000037 · Cited by 27
Neuroimmune nexus of depression and dementia: Shared mechanisms and therapeutic targets
Herman, F. J., Simkovic, S. J., & Pasinetti, G. M. (2019) · British Journal of Pharmacology · doi:10.1111/bph.14569 · Cited by 29
Frank, M. G., Annis, J. L., Watkins, L. R., & Maier, S. F. (2019) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2019.05.014 · Cited by 28
“, 1993), in the context of environmental challenge, the immunological effects of endogenous GCs are more nuanced (Sorrells et al., 2009).”
BackgroundWijenayake, S., Rahman, M. F., Lum, C. M. W., de Vega, W. C., Sasaki, A., & McGowan, P. O. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01798-1 · Cited by 31
The role of the stress system in recovery after traumatic brain injury: A tribute to Bruce S. McEwen
Weil, Z. M., White, B. A., Whitehead, B. J., & Karelina, K. (2022) · Neurobiology of Stress · doi:10.1016/j.ynstr.2022.100467 · Cited by 29
How does epidermal pathology interact with mental state?
Denda, M., Takei, K., & Denda, S. (2012) · Medical Hypotheses · doi:10.1016/j.mehy.2012.11.027 · Cited by 28
Steroid Profiling in Male Wobbler Mouse, a Model of Amyotrophic Lateral Sclerosis
Deniselle, M. C. G., Lière, P., Pianos, A., Meyer, M., Aprahamian, F., Cambourg, A., Giorgio, N. P. D., Schumacher, M., Nicola, A. F. D., & Guennoun, R. (2016) · Endocrinology · doi:10.1210/en.2016-1244 · Cited by 27
“In the stressed brain, gluco-corticoids can exacerbate inflammation (24).”
BackgroundMasciullo, L., Viscardi, M. F., Piacenti, I., Scaramuzzino, S., CAVALLI, A., Piccioni, M. G., & Porpora, M. G. (2021) · Minerva Obstetrics and Gynecology · doi:10.23736/s2724-606x.21.04779-1 · Cited by 25
Glucocorticoids and Preterm Hypoxic-Ischemic Brain Injury: The Good and the Bad
Bennet, L., Davidson, J. O., Koome, M. E., & Gunn, A. J. (2012) · Journal of Pregnancy · doi:10.1155/2012/751694 · Cited by 26
Stress, Depression, Resilience and Ageing: A Role for the LPA-LPA1 Pathway
Moreno‐Fernández, R. D., Tabbai, S., Castilla‐Ortega, E., Pérez‐Martín, M., Estivill‐Torrús, G., Fernando, R. D. F., Santín, L. J., & Pedraza, C. (2017) · Current Neuropharmacology · doi:10.2174/1570159x15666170710200352 · Cited by 26
“The absence of the LPA1 receptor changes the structure and plasticity of the CNS, with particularly strong effects on the hippocampus [12, 13, 117, 120], mPFC and amygdala [11, 14] as revealed by the behavioural outcome in null mice.”
BackgroundStress, psychiatric disorders, molecular targets, and more
Atrooz, F., Liu, H., & Salim, S. (2019) · Progress in molecular biology and translational science · doi:10.1016/bs.pmbts.2019.06.006 · Cited by 27
Pereira, V. S., Joca, S. R. L., Harvey, B. H., Elfving, B., & Wegener, G. (2019) · Acta Neuropsychiatrica · doi:10.1017/neu.2019.25 · Cited by 23
Srinivasan, M., & Walker, C. L. (2022) · ASN NEURO · doi:10.1177/17590914221120190 · Cited by 25
“However, considerable evidence suggests that the absolute levels of corticosterone as well as the circadian rhythm and ultradian pulsing of GC modulate cellular responses (Dickmeis et al., 2013; Juszczak & Stankiewicz, 2018; Sorrells et al., 2009).”
BackgroundHains, L. E., Loram, L. C., Taylor, F. R., Strand, K. A., Wieseler, J. L., Barrientos, R. M., Young, J. J., Frank, M. G., Sobesky, J. L., Martin, T. J., et al. (2011) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2011.08.011 · Cited by 25
“While glucocorticoids are classically known to be anti-inflammatory, recent evidence from our laboratory and others (Alexander et al., 2009; Sorrells et al., 2009; Frank et al., 2010; Loram et al., 2011) have identified that when CORT is administered before a subsequent immune challenge, the proinflammatory response i…”
BackgroundDaniilidou, M., Holleman, J., Hagman, G., Kåreholt, I., Aspö, M., Brinkmalm, A., Zetterberg, H., Blennow, K., Solomon, A., Kivipelto, M., et al. (2024) · Translational Psychiatry · doi:10.1038/s41398-024-03072-x · Cited by 27
Chijiwa, T., Oka, T., Lkhagvasuren, B., Yoshihara, K., & Sudo, N. (2015) · Physiology & Behavior · doi:10.1016/j.physbeh.2015.04.050 · Cited by 24
“Interestingly, several studies have reported that stress-induced secretion of glucocorticoids (GCs) plays a pivotal role in microglial priming as an alarm signal of danger [17–19].”
BackgroundFeltes, P. K., de Vries, E. F. J., Juárez‐Orozco, L. E., Kurtys, E., Dierckx, R., Jeckel, C. M. M., & Doorduin, J. (2017) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1177/0271678x17747189 · Cited by 24
Charles, M. S., Ostrowski, R. P., Manaenko, A., Ďuriš, K., Zhang, J. H., & Tang, J. (2012) · Neurobiology of Disease · doi:10.1016/j.nbd.2012.03.021 · Cited by 24
“Glucocorticoids are reported to play an important role in neurological function (Dumas et al., 2010; Sorrells et al., 2009), and neuronal damage in the hippocampus after ischemic insults (Roy and Sapolsky, 2003).”
BackgroundBacterial lipopolysaccharide induces type 2 deiodinase in cultured rat astrocytes
Lamirand, A., Ramaugé, M., Pierre, M., & Courtin, F. (2010) · Journal of Endocrinology · doi:10.1677/joe-10-0218 · Cited by 24
“Moreover, emerging literature suggests that glucocorticoid pro-inflammatory effects can co-exist with their anti-inflammatory properties, particularly in the central nervous system (Sorrells et al. 2009).”
BackgroundMulti-Systemic Biological Risk and Cancer Mortality: The NHANES III Study
Acheampong, T., Jiang, L., Ziogas, A., & Odegaard, A. (2020) · Scientific Reports · doi:10.1038/s41598-020-61945-9 · Cited by 28
Network between Cytokines, Cortisol and Occupational Stress in Gas and Oilfield Workers
Reale, M., Costantini, E., D’Angelo, C., Coppeta, L., Mangifesta, R., Jagarlapoodi, S., Nicola, M. D., & Giampaolo, L. D. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21031118 · Cited by 28
“Dysregulation of the HPA axis results in the lack of suppression of the immune system, known as glucocorticoid resistance [7].”
BackgroundPsychological Stress as a Modulator of Functional Recovery Following Spinal Cord Injury
Bouchard, S. M., & Hook, M. A. (2014) · Frontiers in Neurology · doi:10.3389/fneur.2014.00044 · Cited by 26
Modulation of Hippocampal Antioxidant Defense System in Chronically Stressed Rats by Lithium
Popović, N., Stojiljković, V., Pejić, S., Todorović, A., Pavlović, I., Gavrilović, L., & Pajović, S. B. (2019) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2019/8745376 · Cited by 22
“Chronic stress induces overactivation and dysfunction of stress-activated systems, resulting in further brain damage and mood disorders [3, 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
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