Research progress of neuroinflammation-related cells in traumatic brain injury: A review

Zhao, Qinghui; Li, Huige; Li, Hongru; Xie, Fei; Zhang, Jianhua

doi:10.1097/md.0000000000034009

Cited by 4 publications

References 130 publications

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Short-chain fatty acids are a key mediator of gut microbial regulation of T cell trafficking and differentiation after traumatic brain injury

Celorrio,

Shumilov,

et al. 2024

Preprint

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The gut microbiota has emerged as a pivotal regulator of host inflammatory processes after traumatic brain injury (TBI). However, the mechanisms by which the gut microbiota communicates to the brain in TBI are still under investigation. We previously reported that gut microbiota depletion (GMD) using antibiotics after TBI resulted in increased microglial activation, reduced neurogenesis, and reduced T cell infiltration. In the present study, we have demonstrated that intestinal T cells contribute to the pool of cells infiltrating the brain after TBI. Depletion or genetic deletion of T cells before injury reversed GMD induced reductions in post-TBI neurogenesis. Short-chain fatty acid supplementation increased T regulatory and T helper1 cell infiltration to the brain along with restoring neurogenesis and microglia activation after TBI with GMD. These data suggest that T cell subsets are essential cellular mediators by which the gut microbiota modulates TBI pathogenesis, a finding with important therapeutic implications.

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Short-chain fatty acids are a key mediator of gut microbial regulation of T cell trafficking and differentiation after traumatic brain injury

Celorrio,

Shumilov,

et al. 2024

Preprint

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Utility of systemic immune-inflammation index, neutrophil-to-lymphocyte ratio, and platelet-to-lymphocyte ratio as a predictive biomarker in pediatric traumatic brain injury

Parenrengi,

Suryaningtyas,

Dariansyah

et al. 2024

Surgical Neurology International

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Background: Traumatic brain injury (TBI) remains the predominant cause of mortality and disability among the pediatric population. At present, there are no radiation-free, simple, and cost-effective tools available to assess the severity and prognosis of pediatric TBI. The systemic immune-inflammation index (SII), neutrophilto-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio (PLR) serve as inflammatory biomarkers that may assist in predicting the outcome of pediatric TBI. This research aims to assess the utility of SII, NLR, and PLR as a predictive biomarker in children with TBI. Methods: A retrospective analysis was conducted on SII, NLR, and PLR by reviewing the medical records of all pediatric (age ≤18 years) TBI cases who came to the emergency department in the period from January 2023 to August 2024. Patients were categorized according to 28-day mortality and the severity of TBI. The correlation between the biomarkers and outcomes was analyzed. Results: A total of 206 patients were included in this study. The mean age was 13.81 (1–18). The 28-day mortality rate was 5.3% (n = 11). There were no significant differences in SII, NLR, and PLR between the survivor and mortality groups (P = 0.317, P = 0.288, and P = 0.200, respectively). Based on the TBI severity, there was a significant difference in the SII, NLR, and PLR across mild, moderate, and severe TBI (P = 0.006, P = 0.002, P = 0.001, respectively). Conclusion: The findings of our study did not reveal a significant predictive relationship between SII, NLR, and PLR to 28-day mortality. Nonetheless, there were significant differences in SII, NLR, and PLR among mild, moderate, and severe TBI groups. Further research under more controlled conditions is essential to facilitate the use of SII, NLR, and PLR as predictive biomarkers in pediatric TBI.

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Antioxidant and Anti-Inflammatory Properties of Melatonin in Secondary Traumatic Brain Injury

Sieminski,

Reimus,

Kałas

et al. 2024

Antioxidants

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Traumatic brain injury (TBI) is a disease resulting from external physical forces acting against the head, leading to transient or chronic damage to brain tissue. Primary brain injury is an immediate and, therefore, rather irreversible effect of trauma, while secondary brain injury results from a complex cascade of pathological processes, among which oxidative stress and neuroinflammation are the most prominent. As TBI is a significant cause of mortality and chronic disability, with high social costs all over the world, any form of therapy that may mitigate trauma-evoked brain damage is desirable. Melatonin, a sleep–wake-cycle-regulating neurohormone, exerts strong antioxidant and anti-inflammatory effects and is well tolerated when used as a drug. Due to these properties, it is very reasonable to consider melatonin as a potential therapeutic molecule for TBI treatment. This review summarizes data from in vitro studies, animal models, and clinical trials that focus on the usage of melatonin in TBI.

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Research progress of neuroinflammation-related cells in traumatic brain injury: A review

Cited by 4 publications

References 130 publications

Short-chain fatty acids are a key mediator of gut microbial regulation of T cell trafficking and differentiation after traumatic brain injury

Short-chain fatty acids are a key mediator of gut microbial regulation of T cell trafficking and differentiation after traumatic brain injury

Utility of systemic immune-inflammation index, neutrophil-to-lymphocyte ratio, and platelet-to-lymphocyte ratio as a predictive biomarker in pediatric traumatic brain injury

Antioxidant and Anti-Inflammatory Properties of Melatonin in Secondary Traumatic Brain Injury

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