Kassner Stefan S, Schöttler Sarah, Bonaterra Gabriel A, Stern-Straeter Jens, Hormann Karl, Kinscherf Ralf, Gössler Ulrich R
Department of Otorhinolaryngology, Head and Neck Surgery, University Hospital Mannheim, Mannheim, Germany.
Audiol Neurootol. 2011;16(4):242-7. doi: 10.1159/000320839. Epub 2010 Oct 28.
Vestibular neuritis (VN) is characterized by acute vertigo with spontaneous nystagmus and is often accompanied by vegetative symptoms. While the pathogenetic process leading to this disease is widely unknown, increasing evidence exists that a proinflammatory environment is responsible for the induction and progression of VN. Twelve patients with acute VN and 12 healthy, age-matched individuals were included in this study. In addition to routine blood parameters, plasma levels of soluble CD40 receptor/ligand (sCD40/sCD40L) were determined by ELISA. Moreover, peripheral blood mononuclear cells (PBMCs) were isolated by Ficoll density gradient. Afterwards, in CD14 (monocytes), CD68 (macrophages), CD3 (T lymphocytes) or CD19 (B lymphocytes) subpopulations, proinflammatory [CD40, tumor necrosis factor-α (TNF-α), and COX-2], proapoptotic [caspase-3, and poly(adenosine diphosphate ribose) polymerase] and proadhesive (CD38) proteins were measured by 2-color fluorescence-activated cell sorter analyses. In comparison to healthy individuals, patients with acute VN revealed significantly elevated plasma levels of C-reactive protein, whereas plasma levels of sCD40 and sCD40L, as well as cholesterol/triglyceride status were similar. However, we found a significant elevation of the percentage of proinflammatory CD40+, TNF-α+, COX-2+ or CD38+ PBMCs. Elevation of proinflammatory and proadhesive proteins in PBMCs of patients with acute VN in parallel with an acute phase response may contribute to disease induction and progression and, thus, may be suggested as a novel therapeutic target.
前庭神经炎（VN）的特征是急性眩晕伴自发性眼球震颤，常伴有自主神经症状。虽然导致这种疾病的发病机制尚不清楚，但越来越多的证据表明，促炎环境是VN发生和发展的原因。本研究纳入了12例急性VN患者和12名年龄匹配的健康个体。除了常规血液参数外，通过酶联免疫吸附测定法（ELISA）测定可溶性CD40受体/配体（sCD40/sCD40L）的血浆水平。此外，通过Ficoll密度梯度分离外周血单核细胞（PBMC）。随后，在CD14（单核细胞）、CD68（巨噬细胞）、CD3（T淋巴细胞）或CD19（B淋巴细胞）亚群中，通过双色荧光激活细胞分选分析测定促炎蛋白[CD40、肿瘤坏死因子-α（TNF-α）和COX-2]、促凋亡蛋白[半胱天冬酶-3和聚（二磷酸腺苷核糖）聚合酶]和促黏附蛋白（CD38）。与健康个体相比，急性VN患者的C反应蛋白血浆水平显著升高，而sCD40和sCD40L的血浆水平以及胆固醇/甘油三酯状态相似。然而，我们发现促炎的CD40+、TNF-α+、COX-2+或CD38+PBMC的百分比显著升高。急性VN患者PBMC中促炎和促黏附蛋白的升高与急性期反应同时出现，可能有助于疾病的发生和发展，因此，可作为一个新的治疗靶点。
