Department of Neurology, Medical University of Białystok, Białystok, Poland.
Neurodegener Dis. 2011;8(5):375-80. doi: 10.1159/000324373. Epub 2011 Mar 10.
BACKGROUND/AIMS: Cell damage during the course of inflammation results in cytoplasmic actin release, which if not eliminated by the extracellular actin scavenger system, composed of gelsolin and vitamin D binding protein, can cause dysfunction of hemostasis and toxicity towards surrounding cells. In this study, we test the hypothesis that an inflammatory reaction induced by central nervous system infections such as tick-borne encephalitis (TBE) or Lyme neuroborreliosis (LNB) will result in plasma gelsolin concentration changes in the blood and cerebrospinal fluid (CSF).
Quantitative Western blot was used to determine gelsolin levels in 58 samples, which include: 29 patients without infection (diagnosed with conditions such as idiopathic cephalalgia, idiopathic Bell's facial nerve palsy and ischialgia due to discopathy in which standard CSF diagnostic tests show no abnormalities), 12 patients diagnosed with TBE, and 17 patients diagnosed with LNB sub forma meningitis.
The gelsolin concentration in the blood of patients with TBE (163.2 ± 80.8 μg/ml) and LNB (113.6 ± 56.8 μg/ml) was significantly lower (p < 0.05 and p < 0.001, respectively) compared to the control group (226.3 ± 100.7 μg/ml). Furthermore, there was no statistically significant difference between the CSF gelsolin concentration in patients with TBE (3.9 ± 3.3 μg/ml), LNB (2.9 ± 1.2 μg/ml) and the control group (3.7 ± 3.3 μg/ml). An observed decrease in gelsolin concentration in the blood of TBE and LNB patients supports previous findings indicating the involvement of gelsolin in the pathophysiology of an inflammatory response. Therefore, evaluation of blood gelsolin concentration and administration of recombinant plasma gelsolin might provide a new tool to develop diagnostic and therapeutic strategies for TBE and LNB.
背景/目的：炎症过程中的细胞损伤导致细胞质肌动蛋白释放，如果不被细胞外肌动蛋白清除系统（由胶凝蛋白和维生素 D 结合蛋白组成）清除，可能导致止血功能障碍和对周围细胞的毒性。在这项研究中，我们检验了这样一个假设，即中枢神经系统感染（如蜱传脑炎（TBE）或莱姆神经Borreliosis（LNB））引起的炎症反应将导致血液和脑脊液（CSF）中血浆胶凝蛋白浓度的变化。
使用定量 Western blot 法测定 58 例样本中的胶凝蛋白水平，包括：29 例无感染患者（诊断为特发性头痛、特发性贝尔面神经麻痹和椎间盘病变引起的坐骨神经痛，这些疾病的标准 CSF 诊断测试无异常），12 例 TBE 患者和 17 例 LNB 亚形式脑膜炎患者。
TBE（163.2 ± 80.8 μg/ml）和 LNB（113.6 ± 56.8 μg/ml）患者的血液胶凝蛋白浓度明显低于对照组（分别为 p < 0.05 和 p < 0.001）（226.3 ± 100.7 μg/ml）。此外，TBE（3.9 ± 3.3 μg/ml）和 LNB（2.9 ± 1.2 μg/ml）患者 CSF 胶凝蛋白浓度与对照组（3.7 ± 3.3 μg/ml）之间无统计学差异。TBE 和 LNB 患者血液胶凝蛋白浓度的降低支持了先前的研究结果，表明胶凝蛋白参与了炎症反应的病理生理学过程。因此，评估血液胶凝蛋白浓度和给予重组血浆胶凝蛋白可能为开发 TBE 和 LNB 的诊断和治疗策略提供新的工具。
