| Literature DB >> 35969281 |
Yuwen Chen1,2, Ying Wang1,2, Jian Xu3, Tingting Hou1,4, Jing Zhu1,2, Yingzi Jiang1,2, Liying Sun5, Chunling Huang1,2, Lulu Sun1,2, Su Liu6.
Abstract
Chemokines may promote neuroinflammation following traumatic brain injury (TBI), thereby exacerbating secondary injury. This study was designed to investigate the contributions of chemokines (CCL2, CCL5, CXCL1, CXCL10, and CXCL13) to TBI severity and clinical outcome. Peripheral blood was drawn from 92 TBI patients on admission, and 40 controls were recruited. Serum concentrations of CCL2, CCL5, CXCL1, CXCL10, and CXCL13 on admission were measured by ELISA. Preoperative clinical severity was evaluated using the Glasgow Coma Scale (GCS), and clinical outcome at 90 days post-TBI was evaluated using the Glasgow Outcome Scale (GOS). The associations were evaluated by calculating Spearman's correlation coefficients. A binary logistic regression model was used to identify clinicodemographic factors influencing outcome, and ROC curves were constructed. Serum concentrations of CCL2, CCL5, CXCL1, CXCL10, and CXCL13 were elevated significantly after TBI and negatively correlated with GCS and GOS scores except CCL5. CCL2 may be considered as an independent predictor to predict severity and outcome. Moreover, combination of GCS score, CCL2, and CXCL10 can be a better assessment prognosis of moderate and severe TBI.Entities:
Keywords: CCL2; CXCL10; CXCL13; Neuroinflammation; Traumatic brain injury
Year: 2022 PMID: 35969281 DOI: 10.1007/s10753-022-01729-7
Source DB: PubMed Journal: Inflammation ISSN: 0360-3997 Impact factor: 4.657