СХС-CHEMOKINE DETECTION IN THE CSF OF PATIENTS WITH BRAIN CONTUSIONS

Abstract

Traumatic brain injury (TBI) is among the most significant forms of neurological pathology. In traumatic brain injury, axonal damage occurs not only as a result of direct cytotoxic intercellular interactions but also due to the activation of pro-inflammatory cytokines and chemokines, which play a crucial role in the development and maintenance of neuroinflammation. In the early stages after brain trauma, there is not only activation of microglia but also formation of a pool of T-cell subpopulations capable of synthesizing various chemokines. The aim of this study was to comprehensively assess the concentration of chemokines (CXCL8/MIG, CXCL9/IP-10, CXCL10/I-TAC) in the cerebrospinal fluid (CSF) of patients with brain contusion of varying severity within the first 24 hours after hospital admission. The study included 86 patients diagnosed with "TBI: brain contusion," who were divided into three groups based on injury severity. A comparison group consisted of patients with concussion (n=24). Obtaining CSF from healthy individuals is challenging due to the absence of indications for lumbar puncture procedures. Chemokine concentrations (pg/mL) were measured using multiplex analysis based on xMAP technology (Luminex), utilizing Milliplex MAP test systems (Millipore, USA). The results showed a trend toward increased chemokine levels correlating with greater injury severity. Notably, CXCL9/MIG levels were elevated in all patients with brain injury (p<0.05), unlike CXCL8/IL-8, which showed significant increases only in the fourth group (severe TBI), and CXCL10/IP-10, which was significantly elevated in both the third (moderate TBI) and fourth groups. Specifically, in the fourth group (severe TBI), levels of CXCL8/IL-8 were increased 3.5 times, CXCL9/MIG – 9 times, and CXCL10/IP-10 – 3 times compared to the control group (first group with mild TBI). To evaluate the diagnostic value of these changes, ROC analysis was performed, establishing clinically significant chemokine thresholds that serve as highly informative markers of neural tissue damage. In conclusion, assessing levels of CXCL8, CXCL9, and CXCL10 in brain contusion provides valuable insights into their roles in disease progression — recruiting T-helper cells and neutrophils from peripheral blood into neural tissue and sustaining neuroinflammatory processes.