ArticleBrain, behavior, and immunity2011
Prior exposure to glucocorticoids potentiates lipopolysaccharide induced mechanical allodynia and spinal neuroinflammation.
Article in Brain, behavior, and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
34 citing papers in PubMed, 57 citations in OpenAlex.
- The different mechanisms of peripheral and central TLR4 on chronic postsurgical pain in rats.Journal of anatomy · 2021Article
- Glucocorticosteroids Effects on Brain Development in the Preterm Infant: A Role for Microglia?Current neuropharmacology · 2021Review
- Glucocorticoids mediate stress induction of the alarmin HMGB1 and reduction of the microglia checkpoint receptor CD200R1 in limbic brain structures.Brain, behavior, and immunity · 2019Article
- Corticosterone and pyridostigmine/DEET exposure attenuate peripheral cytokine expression: Supporting a dominant role for neuroinflammation in a mouse model of Gulf War Illness.Neurotoxicology · 2019Article
- Stress and aging act through common mechanisms to elicit neuroinflammatory priming.Brain, behavior, and immunity · 2018Review
- Stress disinhibits microglia via down-regulation of CD200R: A mechanism of neuroinflammatory priming.Brain, behavior, and immunity · 2018Article
- Modulating the Oxytocin System During the Perinatal Period: A New Strategy for Neuroprotection of the Immature Brain?Frontiers in neurology · 2018Review
- Prior exposure to corticosterone markedly enhances and prolongs the neuroinflammatory response to systemic challenge with LPS.PloS one · 2018Article
- Glial and neuroinflammatory targets for treating substance use disorders.Drug and alcohol dependence · 2017Review
- Corticosterone and exogenous glucose alter blood glucose levels, neurotoxicity, and vascular toxicity produced by methamphetamine.Journal of neurochemistry · 2017Article
- Corticosterone primes the neuroinflammatory response to Gulf War Illness-relevant organophosphates independently of acetylcholinesterase inhibition.Journal of neurochemistry · 2017Article
- Lifetime Modulation of the Pain SystemFrontiers in immunology · 2017Review
- Systemic TAK-242 prevents intrathecal LPS evoked hyperalgesia in male, but not female mice and prevents delayed allodynia following intraplantar formalin in both male and female mice: The role of TLR4 in the evolution of a persistent pain state.Brain, behavior, and immunity · 2016Article
- Inhibition of the Rho/Rho kinase pathway prevents lipopolysaccharide-induced hyperalgesia and the release of TNF-α and IL-1β in the mouse spinal cord.Scientific reports · 2015Article
- Corticosterone primes the neuroinflammatory response to DFP in mice: potential animal model of Gulf War Illness.Journal of neurochemistry · 2015Article
- Select steroid hormone glucuronide metabolites can cause toll-like receptor 4 activation and enhanced pain.Brain, behavior, and immunity · 2015Article
- High-fat diet consumption disrupts memory and primes elevations in hippocampal IL-1β, an effect that can be prevented with dietary reversal or IL-1 receptor antagonism.Brain, behavior, and immunity · 2014Article
- Article
- Glucocorticoids regulate natural killer cell function epigenetically.Cellular immunology · 2014Article
- Pathological pain and the neuroimmune interface.Nature reviews. Immunology · 2014Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
While stress and stress-induced glucocorticoids are classically considered immunosuppressive, they can also enhance proinflammatory responses to subsequent challenges. Corticosterone (CORT) primes rat immune cells, exacerbating pro-inflammatory responses to subsequent immune challenges. Stress can also sensitize pain. One possibility is that stress primes spinal immune cells, predominantly glia, which are key mediators in pain enhancement through their release of proinflammatory cytokines. Therefore, we aimed to identify whether prior CORT sensitizes spinal cord glia such that a potentiated pro-inflammatory response occurs to later intrathecal (IT) lipopolysaccharide (LPS), thereby enhancing pain. Rats received subcutaneous CORT/vehicle 24 h before IT LPS/vehicle. Hind paw pain thresholds were measured before CORT/vehicle, before and up to 48 h after IT LPS/vehicle. In separate rats treated as above, lumbar spinal cord tissue was collected and processed for proinflammatory mediators. CORT alone had no effect on pain responses, nor on any pro-inflammatory cytokines measured. LPS induced allodynia (decreased pain threshold) lasting <4 h and elevated spinal IL-1β and IL-6 protein. Prior CORT potentiated allodynia, lasting >24 h following LPS and potentiated spinal IL-1 and IL-6 protein. Coadministration of IL-1 receptor antagonist with LPS IT completely blocked the allodynia irrespective of whether the system was primed by CORT or not. At 24 h, TLR2, TLR4, MD2, and CD14 mRNAs were significantly elevated within the spinal cord in the CORT+LPS group compared to all other groups. Prior CORT before a direct spinal immune challenge is able to potentiate pain responses and pro-inflammatory cytokine production.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.