Background: Severe traumatic brain injuries (STBIs) cause 1/3-1/2 of trauma-related deaths. Tumor necrosis factor (TNF) receptor-associated factor NF-κB activator (TANK)-binding kinase 1 (TBK1) is a biomarker associated with inflammation, while inflammation is a key promoter of the TBI process.
Objectives: To investigate the clinical significance of TBK1 in STBI patients.
Material And Methods: The present prospective observational study included a total of 95 STBI cases diagnosed from October 2019 to October 2021. The values for optic nerve sheath diameter (ONSD) were determined under deep sedation using 2-dimensional gray scale ultrasound. Intracranial pressure (ICP) was also measured. Serum levels of TBK1 and inflammatory factors such as C-reactive protein (CRP), interleukin (IL)-1β and IL-6 were evaluated with enzyme-linked immunosorbent assay (ELISA). Clinical variables including pathological type, Glasgow Coma Scale (GCS) score, sequential organ failure assessment (SOFA) score, and Acute Physiology and Chronic Health Evaluation II (APACHE II) score were recorded.
Results: The levels of TBK1 in the deceased patients were remarkably lower than in the patients who survived. The IL-1β and IL-6 were markedly elevated in deceased patients compared with survivors, and negatively correlated with serum levels of TBK1. The ONSD and ICP values were significantly higher in the deceased patients than in the patients who survived and were positively correlated with each other, while both were negatively correlated with TBK1 levels. Patients with lower TBK1 expression showed significantly lower GCS scores, higher SOFA and APACHE II scores, as well as a higher 1-month mortality rate. The Kaplan-Meier curve showed that patients with higher TBK1 levels had a higher 1-month survival rate compared with the patients with lower TBK1 levels. Only TBK1 and ONSD were independent risk factors for 1-month mortality in STBI patients.
Conclusions: Lower serum TBK1 levels are associated with higher inflammatory factors, higher ONSD and ICP levels, as well as a poorer prognosis in STBI patients.
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http://dx.doi.org/10.17219/acem/155040 | DOI Listing |
Front Pharmacol
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College of Pharmacy, Yanbian University Hospital, Yanbian University, Yanji, China.
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Rheumatology Unit, Department of Clinical Internal, Anesthesiologic and Cardiovascular Sciences, "Sapienza" University of Rome, Rome, Italy.
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Department of Breast Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
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Department of Anesthesiology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou, Hainan Province 570311, China. Electronic address:
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National Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China.
Innate immunity serves as a crucial defense mechanism against invading pathogens, yet its negative regulatory network remains under explored. In this study, we identify BEN domain-containing protein 6 (BEND6) as a novel negative regulator of innate immunity through a genome-scale CRISPR knockout screen for host factors essential for viral replication. We show that BEND6 exhibits characteristics of an interferon-stimulated gene (ISG), with its mRNA and protein levels upregulated by RNA virus-induced IFN-β.
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