ArticleBrain, behavior, and immunity2012
Beta adrenergic blockade decreases the immunomodulatory effects of social disruption stress.
Article in Brain, behavior, and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06263452 (Beta-Blocker Influences on Inflammatory and Neural Responses to Stress), which is not on this map. Cited by 85 papers, 1 of them a synthesis that pooled it.
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.
Beta-Blocker Influences on Inflammatory and Neural Responses to Stress
Who cites it
85 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.
- Glucocorticoid resistance and β2-adrenergic receptor signaling pathways promote peripheral pro-inflammatory conditions associated with chronic psychological stress: A systematic review across species.Neuroscience and biobehavioral reviews · 2021Pooled it
- The effect of beta-adrenergic blockade on inflammatory and cardiovascular responses to acute mental stress.Brain, behavior, and immunity · 2018Trial
- Biopsychosocial influence on shoulder pain: Rationale and protocol for a pre-clinical trial.Contemporary clinical trials · 2017Trial
- Trial
- The therapeutic effects of labetalol in chronic stress- and immuno-agonist-induced cough hypersensitivity and lung inflammation involve reducing interferon-γ-producing T lymphocytes.ERJ open research · 2026Article
- Social stress worsens colitis through β-adrenergic-driven oxidative stress in intestinal mucosal compartments.Brain, behavior, and immunity · 2026Article
- Chronic sensory contact with subordinated conspecifics promotes splenic glucocorticoid resistance in experimentally wounded C57BL/6N male mice.Scientific reports · 2024Article
- Antagonism of the brain P2X7 ion channel attenuates repeated social defeat induced microglia reactivity, monocyte recruitment and anxiety-like behavior in male mice.Brain, behavior, and immunity · 2024Article
- Article
- The Interaction between Psychological Stress and Iron Status on Early-Life Neurodevelopmental Outcomes.Nutrients · 2023Review
- Repeated mild traumatic brain injury in mice elicits long term innate immune cell alterations in blood, spleen, and brain.Journal of neuroimmunology · 2023Article
- Animal Inflammation-Based Models of Neuropsychiatric Disorders.Advances in experimental medicine and biology · 2023Article
- The neuroimmunology of social-stress-induced sensitization.Nature immunology · 2022Review
- Microglia as Central Protagonists in the Chronic Stress Response.Neurology(R) neuroimmunology & neuroinflammation · 2022Review
- Effect of chronic stress on tumorigenesis and development.Cellular and molecular life sciences : CMLS · 2022Review
- The role of the immune system in posttraumatic stress disorder.Translational psychiatry · 2022Review
- Review
- Using Mice to Model Human Disease: Understanding the Roles of Baseline Housing-Induced and Experimentally Imposed Stresses in Animal Welfare and Experimental Reproducibility.Animals : an open access journal from MDPI · 2022Review
- Psychological stress creates an immune suppressive environment in the lung that increases susceptibility of aged mice toFrontiers in cellular and infection microbiology · 2022Article
- Adrenergic signaling regulation of macrophage function: do we understand it yet?Immunotherapy advances · 2022Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
During physiological or psychological stress, catecholamines produced by the sympathetic nervous system (SNS) regulate the immune system. Previous studies report that the activation of β-adrenergic receptors (βARs) mediates the actions of catecholamines and increases pro-inflammatory cytokine production in a number of different cell types. The impact of the SNS on the immune modulation of social defeat has not been examined. The following studies were designed to determine whether SNS activation during social disruption stress (SDR) influences anxiety-like behavior as well as the activation, priming, and glucocorticoid resistance of splenocytes after social stress. CD-1 mice were exposed to one, three, or six cycles of SDR and HPLC analysis of the plasma and spleen revealed an increase in catecholamines. After six cycles of SDR the open field test was used to measure behaviors characteristic of anxiety and indicated that the social defeat induced increase in anxiety-like behavior was blocked by pre-treatment with the β-adrenergic antagonist propranolol. Pre-treatment with the β-adrenergic antagonist propranolol did not significantly alter corticosterone levels indicating no difference in activation of the hypothalamic-pituitary-adrenal axis. In addition to anxiety-like behavior the SDR induced splenomegaly and increase in plasma IL-6, TNFα, and MCP-1 were each reversed by pre-treatment with propranolol. Furthermore, flow cytometric analysis of cells from propranolol pretreated mice reduced the SDR-induced increase in the percentage of CD11b(+) splenic macrophages and significantly decreased the expression of TLR2, TLR4, and CD86 on the surface of these cells. In addition, supernatants from 18h LPS-stimulated ex vivo cultures of splenocytes from propranolol-treated SDR mice contained less IL-6. Likewise propranolol pre-treatment abrogated the glucocorticoid insensitivity of CD11b(+) cells ex vivo when compared to splenocytes from SDR vehicle-treated mice. Together, this study demonstrates that the immune activation and priming effects of SDR result, in part, as a consequence of SNS activation.
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What OpenQuestion holds
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.