ArticleBrain, behavior, and immunity2020
Peripheral inflammation is strongly linked to elevated zero maze behavior in repeated social defeat stress.
Article in Brain, behavior, and immunity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Inflammation as a mediating pathway between social defeat and mental health in humans: A systematic review.Translational psychiatry · 2026Pooled it
- Network-level organization of systemic inflammation reflects early Alzheimer's-like behavioral changes.Scientific reports · 2025Article
- 17β-Trenbolone Increases the Release of Lipocalin 2 via the Brain-Liver Axis and Causes Alzheimer's Disease-Like Symptoms in CSDS-Induced Mice.Molecular neurobiology · 2025Article
- Network-Level Organization of Systemic Inflammation Reflects Early Alzheimer's-Like Behavioral Changes.Research square · 2025Article
- Psychological trauma increases blood pressure sensitivity to angiotensin II via T-lymphocytes independent of psychopathology.bioRxiv : the preprint server for biology · 2025Article
- Psychological trauma increases blood pressure sensitivity to angiotensin II via T-lymphocytes independent of psychopathology.Frontiers in cellular neuroscience · 2025Article
- TBrain, behavior, and immunity · 2025Article
- In a circuit necessary for cognition and emotional affect, Alzheimer's-like pathology associates with neuroinflammation, cognitive and motivational deficits in the young adult TgF344-AD rat.Brain, behavior, & immunity - health · 2024Article
- Stress increases hepatic release of lipocalin 2 which contributes to anxiety-like behavior in mice.Nature communications · 2024Article
- Innate and adaptive immune system consequences of post-traumatic stress disorder.Autonomic neuroscience : basic & clinical · 2024Review
- Repeated social defeat stress leads to immunometabolic shifts in innate immune cells of the spleen.Brain, behavior, & immunity - health · 2023Article
- Repeated Social Defeat Stress Induces an Inflammatory Gut Milieu by Altering the Mucosal Barrier Integrity and Gut Microbiota Homeostasis.Biological psychiatry global open science · 2023Article
- S100a9 Protects Against the Effects of Repeated Social Defeat Stress.Biological psychiatry global open science · 2023Article
- Post-traumatic Stress Disorder: Focus on Neuroinflammation.Molecular neurobiology · 2023Review
- Sex-specific immune mechanisms in PTSD symptomatology and risk: A translational overview and perspectives.Brain research bulletin · 2023Review
- Understanding the Role of Oxidative Stress, Neuroinflammation and Abnormal Myelination in Excessive Aggression Associated with Depression: Recent Input from Mechanistic Studies.International journal of molecular sciences · 2023Review
- Neuroinflammation is a susceptibility factor in developing a PTSD-like phenotype.Frontiers in behavioral neuroscience · 2023Article
- The role of the immune system in posttraumatic stress disorder.Translational psychiatry · 2022Review
- T-lymphocyte tyrosine hydroxylase regulates TBrain, behavior, and immunity · 2022Article
- Inflammation-driven brain and gut barrier dysfunction in stress and mood disorders.The European journal of neuroscience · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Post-traumatic stress disorder (PTSD) is a psychiatric illness that results in an increased risk for a variety of inflammatory diseases. The exact etiology of this increased risk is unknown, and thus several animal models have been developed to investigate the neuroimmune interactions of PTSD. Repeated social defeat stress (RSDS) is an established preclinical model of psychological trauma that recapitulates certain behavioral and inflammatory aspects of human PTSD. Furthermore, RSDS has been utilized to subgroup animals into susceptible and resilient populations based on one specific behavioral phenotype (i.e., social interaction). Herein, we conducted an extensive investigation of circulating inflammatory proteins after RSDS and found significant elevations in various cytokines and chemokines after exposure to RSDS. When categorizing animals into either susceptible or resilient populations based on social interaction, we found no inflammatory or other behavioral differences between these subgroups. Furthermore, correlative analyses found no significant correlation between social interaction parameters and inflammation. In contrast, parameters from the elevated zero maze (EZM) demonstrated significant associations and clustering to five circulating cytokines. When animals were subdivided into susceptible and resilient populations solely based upon combined EZM performance, significant inflammatory differences were evident between these groups. Strikingly, these circulating inflammatory proteins displayed a stronger predictive ability of EZM performance compared to social interaction test performance. These findings provide new insights into inflammatory markers associated with RSDS, and the utility of EZM to effectively group RSDS-exposed mice into populations with differential levels of peripheral inflammation.
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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.