ArticleJournal of neurotrauma2018
Chronic Alterations in Systemic Immune Function after Traumatic Brain Injury.
Article in Journal of neurotrauma, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 144 citations in OpenAlex.
- Systemic inflammation alters the neuroinflammatory response: a prospective clinical trial in traumatic brain injury.Journal of neuroinflammation · 2021Trial
- Sexual Dimorphism in the Microglial Inflammatory Response After Traumatic Brain Injury.Shock (Augusta, Ga.) · 2026Article
- Herpes simplex virus encephalitis following acute brain injury: illustrative cases.Journal of neurosurgery. Case lessons · 2026Article
- Impact-acceleration head injury results in optic neuropathy in the thirteen-lined ground squirrel.Communications biology · 2026Article
- Repeated head impacts establish a senescent cranial bone marrow niche that impairs brain metabolism.Journal of neuroinflammation · 2026Article
- Systemic inflammation and its associations in acute moderate-severe Traumatic Brain Injury: a cross-sectional study.Brain, behavior, & immunity - health · 2026Article
- Repeated Mild Head Injury Establishes a Senescent Cranial Bone Marrow Niche that Impairs Brain Metabolism.bioRxiv : the preprint server for biology · 2026Article
- A conserved monocyte activation program links brain injury to systemic immune adaptation and clinical outcomes.Frontiers in immunology · 2026Article
- Basophils activate splenic B cells and dendritic cells via IL-13 signaling in acute traumatic brain injury.Journal of neuroinflammation · 2025Article
- Article
- Bone marrow-derived emergency monopoiesis drives brain-lung axis injury after traumatic brain injury via IL-1.Journal of neuroinflammation · 2025Article
- Investigation of the Expression, Localization, and Acidosis-Associated Conformational Changes in Connexin 43 in Traumatic Brain Injury with the Development of a Neural Network Model for Assessing Systemic Inflammation.International journal of molecular sciences · 2025Article
- Within and beyond the tumor: Mechanisms of glioblastoma-induced immunosuppression.Neuro-oncology advances · 2025Review
- Immunosuppressive Formulations for Immunological Defense against Traumatic Brain Injury.Advanced healthcare materials · 2025Article
- Association between traumatic brain injury and risk of developing infections in the central nervous system and periphery.Metabolic brain disease · 2025Review
- Dysregulation of neutrophil in sepsis: recent insights and advances.Cell communication and signaling : CCS · 2025Review
- The immunological landscape of traumatic brain injury: insights from pathophysiology to experimental models.Frontiers in neurology · 2025Review
- Effects of Lifetime Exposure to Sports-Related Head Impacts on Brain Injury and Inflammatory Blood Biomarkers Among Former Middle-Aged Athletes.Neurotrauma reports · 2025Article
- Article
- Peripheral immune cell dysregulation following diffuse traumatic brain injury in pigs.Journal of neuroinflammation · 2024Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
There is a compelling link between severe brain trauma and immunosuppression in patients with traumatic brain injury (TBI). Although acute changes in the systemic immune compartment have been linked to outcome severity, the long-term consequences of TBI on systemic immune function are unknown. Here, adult male C57Bl/6 mice underwent moderate-level controlled cortical impact (CCI) or sham surgery, and systemic immune function was evaluated at 1, 3, 7, 14, and 60 days post-injury. Bone marrow, blood, thymus, and spleen were examined by flow cytometry to assess changes in immune composition, reactive oxygen species (ROS) production, phagocytic activity, and cytokine production. Bone marrow derived macrophages (BMDMs) from sham and 60-day CCI mice were cultured for immune challenge studies using lipopolysaccharide (LPS) and interleukin-4 (IL-4) models. Acutely, TBI caused robust bone marrow activation and neutrophilia. Neutrophils and monocytes exhibited impairments in respiratory burst, cytokine production, and phagocytosis; in contrast, ROS levels and pro-inflammatory cytokine production were chronically elevated at 60 days post-injury. Cultures of BMDMs from chronic CCI mice demonstrated defects in LPS- and IL-4-induced polarization when compared with stimulated BMDMs from sham mice. TBI also caused thymic involution, inverted CD4:CD8 ratios, chronic T lymphopenia, greater memory conversion, increased T cell activation, impaired interferon γ induction, and chronically elevated Th1 cytokine and ROS production. Collectively, our in-depth phenotypic and functional analyses demonstrate that TBI induces widespread suppression of innate and adaptive immune responses after TBI. Moreover, at chronic time points, TBI mice exhibit hallmarks of accelerated immune aging, displaying chronic deficits in systemic immune function.
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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.