创伤性脑损伤
脑脊液
趋化因子
医学
病理生理学
内科学
头部受伤
薄壁组织
载脂蛋白E
内分泌学
受体
免疫学
病理
外科
精神科
疾病
作者
Mario Rancan,Nicole Bye,Vivianne I. Otto,O. Trentz,Thomas Kossmann,Stefan Frentzel,Maria Cristina Morganti-Kossmann
标识
DOI:10.1097/01.wcb.0000133470.91843.72
摘要
The potential role of the chemokine Fractalkine (CX 3 CL1) in the pathophysiology of traumatic brain injury (TBI) was investigated in patients with head trauma and in mice after experimental cortical contusion. In control individuals, soluble (s)Fractalkine was present at low concentrations in cerebrospinal fluid (CSF) (12.6 to 57.3 pg/mL) but at much higher levels in serum (21,288 to 74,548 pg/mL). Elevation of sFractalkine in CSF of TBI patients was observed during the whole study period (means: 29.92 to 535.33 pg/mL), whereas serum levels remained within normal ranges (means: 3,100 to 59,159 pg/mL). Based on these differences, a possible passage of sFractalkine from blood to CSF was supported by the strong correlation between blood–brain barrier dysfunction (according to the CSF-/serum-albumin quotient) and sFractalkine concentrations in CSF (R = 0.706; P < 0.01). In the brain of mice subjected to closed head injury, neither Fractalkine protein nor mRNA were found to be augmented; however, Fractalkine receptor (CX 3 CR1) mRNA steadily increased peaking at 1 week postinjury ( P < 0.05, one-way analysis of variance). This possibly implies the receptor to be the key factor determining the action of constitutively expressed Fractalkine. Altogether, these data suggest that the Fractalkine-CX 3 CR1 protein system may be involved in the inflammatory response to TBI, particularly for the accumulation of leukocytes in the injured parenchyma.
科研通智能强力驱动
Strongly Powered by AbleSci AI