Trial reportCritical care medicine2009
Pretreatment with stress cortisol enhances the human systemic inflammatory response to bacterial endotoxin.
Trial report in Critical care medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Hydrocortisone at stress-associated concentrations helps maintain human heart rate variability during subsequent endotoxin challenge.Journal of critical care · 2011Trial
- Mechanisms underlying delirium in patients with critical illness.Frontiers in aging neuroscience · 2024Review
- Article
- Article
- Nutritional supplements formulated to prevent cognitive impairment in animals.Current research in food science · 2022Article
- Glucocorticosteroids Effects on Brain Development in the Preterm Infant: A Role for Microglia?Current neuropharmacology · 2021Review
- Effect of low-dose corticosterone pretreatment on the production of inflammatory mediators in super-low-dose LPS-primed immune cells.Toxicological research · 2021Article
- Hormonal Changes Associated With Intra-Uterine Growth Restriction: Impact on the Developing Brain and Future Neurodevelopment.Frontiers in endocrinology · 2019Review
- Stress and aging act through common mechanisms to elicit neuroinflammatory priming.Brain, behavior, and immunity · 2018Review
- Modulating the Oxytocin System During the Perinatal Period: A New Strategy for Neuroprotection of the Immature Brain?Frontiers in neurology · 2018Review
- A short-term extremely low frequency electromagnetic field exposure increases circulating leukocyte numbers and affects HPA-axis signaling in mice.Bioelectromagnetics · 2016Article
- Glucocorticoids enhance the in vivo migratory response of human monocytes.Brain, behavior, and immunity · 2016Article
- Oxidative Stress after Surgery on the Immature Heart.Oxidative medicine and cellular longevity · 2016Review
- Pioglitazone in adult rats reverses immediate postnatal overfeeding-induced metabolic, hormonal, and inflammatory alterations.Endocrine · 2015Article
- Relative Adrenal Insufficiency in Pediatric Septic Shock.Journal of pediatric intensive care · 2015Review
- Heat stress-induced memory impairment is associated with neuroinflammation in mice.Journal of neuroinflammation · 2015Article
- Glucocorticoids regulate natural killer cell function epigenetically.Cellular immunology · 2014Article
- Effect of perioperative glucocorticoid administration on postoperative complications following esophagectomy: A meta-analysis.Oncology letters · 2014Article
- Glucocorticoids increase excitotoxic injury and inflammation in the hippocampus of adult male rats.Neuroendocrinology · 2014Article
- Prior exposure to glucocorticoids potentiates lipopolysaccharide induced mechanical allodynia and spinal neuroinflammation.Brain, behavior, and immunity · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThere is continuing controversy regarding the effect of glucocorticoids on a systemic inflammatory process. Based ona model of glucocorticoid action that includes both pro- and anti-inflammatory effects, we used the human experimental endotoxemia model to test the hypothesis that a transient elevation of plasma cortisol to stress-associated levels would enhance a subsequent (delayed) systemic inflammatory response to bacterial endotoxin.
designProspective, randomized, double-blind, placebo-controlled clinical investigation.
settingAcademic medical center. SUBJECTS: Thirty-six healthy human volunteers.
interventionsParticipants were randomized to receive a 6-hr intravenous infusion of saline (control), an intermediate dose of cortisol (Cort80; 6.3 mg/hr/70 kg), or a high dose of cortisol (Cort160; 12.6 mg/hr/70 kg) on day 1. On day 2, participants received an intravenous injection of 2 ng/kg Escherichia coli endotoxin followed by serial measurements of plasma cytokine concentrations. MEASUREMENTS AND MAIN
resultsBaseline participant characteristics and cortisol and cytokine concentrations were similar in all three groups. The plasma cortisol response to endotoxemia on day 2 was similar in all three groups. The interleukin-6 response to endotoxemia was significantly increased in the Cort80 Group compared with the control Group (p = .004), whereas the interleukin-10 response was significantly suppressed (p = .034). Corresponding results for the Cort160 Group were not significantly different from control Group values.
conclusionsIn this study, transient elevation of in vivo cortisol concentrations to levels that are observed during major systemic stress enhanced a subsequent, delayed in vivo inflammatory response to endotoxin. This appeared to be a dose-dependent effect that was more prominent at intermediate concentrations of cortisol than at higher concentrations of cortisol.
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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.