ArticleBrain, behavior, and immunity2019
Glucocorticoids mediate stress induction of the alarmin HMGB1 and reduction of the microglia checkpoint receptor CD200R1 in limbic brain structures.
Article in Brain, behavior, and immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- The mechanisms by which hypothalamic neuroinflammation induced by neonatal cerebral ischemia-hypoxia leads to decreased thymic function via the HPA axis.Cell & bioscience · 2026Article
- Adolescent adversity persistently induces proinflammatory HMGB1 signaling and disrupts the basal forebrain cholinergic system in female rats.Neurobiology of stress · 2026Article
- Active coping mitigates the effects of stress on glucocorticoid levels in the prefrontal cortex.Brain, behavior, and immunity · 2025Article
- Ultrastructural features of psychological stress resilience in the brain: a microglial perspective.Open biology · 2024Review
- Microglial responses to inflammatory challenge in adult rats altered by developmental exposure to polychlorinated biphenyls in a sex-specific manner.Neurotoxicology · 2024Article
- A Case Study of Furunculosis following an Ayurvedic Oil Massage, Sudation Therapy, and Lessons to Learn.Case reports in dermatological medicine · 2024Article
- Stress-induced Neuroinflammation of the Spinal Cord is Restrained by Cort113176 (Dazucorilant), A Specific Glucocorticoid Receptor Modulator.Molecular neurobiology · 2024Article
- "NO" Time in Fear Response: Possible Implication of Nitric-Oxide-Related Mechanisms in PTSD.Molecules (Basel, Switzerland) · 2023Review
- CD200 in dentate gyrus improves depressive-like behaviors of mice through enhancing hippocampal neurogenesis via alleviation of microglia hyperactivation.Journal of neuroinflammation · 2023Article
- Review
- Insights into the Potential Impact of Quetiapine on the Microglial Trajectory and Inflammatory Response in Organotypic Cortical Cultures Derived from Rat Offspring.Biomedicines · 2023Article
- Circulating corticosterone levels mediate the relationship between acute ethanol intoxication and markers of NF-κB activation in male rats.Neuropharmacology · 2022Article
- Effects of RU486 in Treatment of Traumatic Stress-Induced Glucocorticoid Dysregulation and Fear-Related Abnormalities: Early versus Late Intervention.International journal of molecular sciences · 2022Article
- Lactobacillus reuteri effects on maternal separation stress in newborn mice.Pediatric research · 2021Article
- Regulation of neuroimmune processes by damage- and resolution-associated molecular patterns.Neural regeneration research · 2021Review
- A role for neuroimmune signaling in a rat model of Gulf War Illness-related pain.Brain, behavior, and immunity · 2021Article
- Analysis of cerebrovascular dysfunction caused by chronic social defeat in mice.Brain, behavior, and immunity · 2020Article
- Article
- Insights into the Therapeutic Potential of Glucocorticoid Receptor Modulators for Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Exposure to stressors primes neuroinflammatory responses to subsequent immune challenges and stress-induced glucocorticoids (GCs) play a mediating role in this phenomenon of neuroinflammatory priming. Recent evidence also suggests that the alarmin high-mobility group box-1 (HMGB1) and the microglial checkpoint receptor CD200R1 serve as proximal mechanisms of stress-induced neuroinflammatory priming. However, it is unclear whether stress-induced GCs play a causal role in these proximal mechanisms of neuroinflammatory priming; this forms the focus of the present investigation. Here, we found that exposure to a severe acute stressor (inescapable tailshock) induced HMGB1 and reduced CD200R1 expression in limbic brain regions and pharmacological blockade of GC signaling (RU486) mitigated these effects of stress. To confirm these effects of RU486, adrenalectomy (ADX) with basal corticosterone (CORT) replacement was used to block the stress-induced increase in GCs as well as effects on HMGB1 and CD200R1. As with RU486, ADX mitigated the effects of stress on HMGB1 and CD200R1. Subsequently, exogenous CORT was administered to determine whether GCs are sufficient to recapitulate the effects of stress. Indeed, exogenous CORT induced expression of HMGB1 and reduced expression of CD200R1. In addition, exposure of primary microglia to CORT also recapitulated the effects of stress on CD200R1 suggesting that CORT acts directly on microglia to reduce expression of CD200R1. Taken together, these findings suggest that GCs mediate the effects of stress on these proximal mechanisms of neuroinflammatory priming.
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