ArticleJournal of neurochemistry2009
Stress hormones collaborate to induce lymphocyte apoptosis after high level spinal cord injury.
Article in Journal of neurochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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.
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.
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Who cites it
56 citing papers in PubMed, 98 citations in OpenAlex.
- Interaction Between 2 Nutraceutical Treatments and Host Immune Status in the Pediatric Critical Illness Stress-Induced Immune Suppression Comparative Effectiveness Trial.JPEN. Journal of parenteral and enteral nutrition · 2017Trial
- Integrative Analysis of Major Depressive Disorder and Ovarian Cancer: From Genetic Association to Single-Cell Mechanisms.Biomedicines · 2026Article
- Peripheral Immune Remodeling After Spinal Cord Injury: Marked by Expansion of CD38Neurology(R) neuroimmunology & neuroinflammation · 2026Observational
- System failure: Systemic inflammation following spinal cord injury.European journal of immunology · 2024Review
- Spinal cord injury enhances lung inflammation and exacerbates immune response following exposure to LPS.Frontiers in immunology · 2024Article
- Elevated levels of IgA and IgG2 in individuals with chronic spinal cord injury.The journal of spinal cord medicine · 2022Observational
- Spinal Cord Injury Impairs Lung Immunity in Mice.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Immune dysfunction after spinal cord injury - A review of autonomic and neuroendocrine mechanisms.Current opinion in pharmacology · 2022Review
- Thoracic VGluT2The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Exploring the vagus nerve and the inflammatory reflex for therapeutic benefit in chronic spinal cord injury.Current opinion in neurology · 2022Review
- Review
- Central nervous system injury-induced immune suppression.Neurosurgical focus · 2022Review
- Review
- Dynamic changes in the systemic immune responses of spinal cord injury model mice.Neural regeneration research · 2021Article
- Acute post-injury blockade of α2δ-1 calcium channel subunits prevents pathological autonomic plasticity after spinal cord injury.Cell reports · 2021Article
- Contribution of Brain Processes to Tissue Loss After Spinal Cord Injury: Does a Pain-Induced Rise in Blood Pressure Fuel Hemorrhage?Frontiers in systems neuroscience · 2021Article
- Splenic sympathetic signaling contributes to acute neutrophil infiltration of the injured spinal cord.Journal of neuroinflammation · 2020Article
- Spinal cord injury causes chronic bone marrow failure.Nature communications · 2020Article
- Immuno-hematologic parameters following rodent spinal cord contusion are negatively influenced by high-fat diet consumption.Journal of neuroimmunology · 2020Article
- Effects of hospital-acquired pneumonia on long-term recovery and hospital resource utilization following moderate to severe traumatic brain injury.The journal of trauma and acute care surgery · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Post-traumatic immune suppression renders individuals with spinal cord injury (SCI) susceptible to infection. Normally, proper immune function is regulated by collaboration between the sympathetic nervous system (SNS) and hypothalamic-pituitary-adrenal (HPA) axis and involves the controlled release of glucocorticoids (GCs) and norepinephrine (NE). Recently, we showed that after high thoracic (T3) SCI, aberrant levels of GCs and NE accumulate in the blood and spleen, respectively. These changes are associated with splenic atrophy, splenic leucopenia, increased intrasplenic caspase 3 levels, and suppressed B lymphocyte function. As GCs boost SNS function, in part by increasing the expression and affinity of beta2 adrenergic receptors (beta2ARs) while simultaneously preventing beta2AR down-regulation, we predicted that surges in stress hormones (i.e., GCs and NE) in the blood and spleen of mice with high-level SCI would act concurrently to adversely affect lymphocyte function and survival. Here, we show that post-SCI concentrations of GCs enhance the sensitivity of lymphocytes to beta2AR stimulation causing an increase in intracellular Bcl-2 interacting mediator of cell death (Bim) and subsequent apoptosis. In vivo, the combined antagonism of GC receptors and beta2ARs significantly diminished lymphocyte Bim levels and SCI-induced splenic lymphopenia. Together, these data suggest that pharmacological antagonists of the HPA/SNS axes should be considered as adjunct therapies for ameliorating post-traumatic immune suppression in quadriplegics and high paraplegics.
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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.