Role of CXCL1 and CCL2 in patients with severe traumatic brain injury

Abstract

Neuroinflammation is considered to be an essential entry point for clinical treatment after traumatic brain injury (TBI). We have found that Chemokine C-C motif ligand 2 (CCL2)-Chemokine C-C motif receptor 2 (CCR2) signaling has deleterious effects on neuronal survival and learning in TBI rats. However, the molecular mechanism of neuroinflammation in TBI patients still remained to be fully characterized. Immunofluorescent staining for Chemokine (C-X-C motif) ligand 1 (CXCL1), CCL2 and their receptors Chemokine (C-X-C motif) receptor 2 (CXCR2), CCR2 expression was performed to analyze the expression and cell location in human neurocytes. Post-traumatic chemokine expressions were analyzed by using ELISA method. Preoperative GCS, GOS and GCS 30 days after operation were assessed to measure the degree of damage, clinical curative effect and prognosis. The relationships between chemokine expression and clinical prognosis were analyzed by univariate analysis. The expression of CXCL1 was elevated in neurons and astrocytes after TBI, while in neuron without injury. CXCL1 in blood was peaking pre-operation (GCS:6–8) and 1 day after operation (GCS:3–5) then gradually decreasing. The CCL2 was mainly was elevated in astroglial and peaking pre-operation (GCS:6–8) and 1 day post-trauma (GCS:3–5). Serum CXCL1, CCL2 concentrations in sTBI(GCS:3–5) group were negatively correlated with GCS and GOS. CXCL1 mainly expressed in neurons and astrocytes after TBI, and in astrocytes of normal brain. CCL2 was mainly co-localized in astrocytes post-trauma. In sTBI(GCS:3-5) group, the higher CXCL1 and CCL2 protein expression mains the more severe damage and worse prognosis.