Proinflammatory and Proadhesive Activation of Lymphocytes and Macrophages in Sudden Sensorineural Hearing Loss
Proinflammatory and Proadhesive Activation of Lymphocytes and Macrophages in Sudden Sensorineural Hearing Loss
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DOI：
10.1159/000320610
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发表时间：
2011-01-01
影响因子：
1.6
通讯作者：
Goessler, Ulrich R.
中科院分区：
文献类型：
--
作者：
Kassner, Stefan S.;Schoettler, Sarah;Goessler, Ulrich R.
尽管突发感音神经性听力损失（SHL）是一种相当常见的疾病，但导致其发病的发病过程却广为人知。越来越多的证据表明免疫调节细胞，尤其是 T 淋巴细胞可能参与其中。本研究包括 12 名急性 SHL 患者和 12 名年龄匹配的健康个体。除常规血液参数外，还通过 ELISA 测定肿瘤坏死因子 α (TNF-α)、可溶性 CD40 (sCD40) 和 sCD40 配体 (sCD40L) 的血浆水平。此外，通过Ficoll密度梯度分离外周血单个核细胞。然后，在由 CD14（单核细胞）、CD68（巨噬细胞）、CD3（T 淋巴细胞）或 CD19（B 淋巴细胞）免疫反应性鉴定的亚群中，通过 2 色荧光激活细胞分选仪分析测量促炎性（CD40、TNF-α 或环氧合酶-2）和促粘附（CD38）蛋白。与健康个体相比，急性SHL患者的血浆sCD40和sCD40L水平升高，淋巴细胞百分比（36%）显着下降，尤其是T淋巴细胞（28%）。此外，在急性 SHL 患者中，促炎性 CD40、TNF-α、环氧合酶-2 或 CD38 阳性 T 或 B 淋巴细胞的百分比显着增加。我们的数据表明外周循环中促粘附和促炎淋巴细胞的外渗增强，这可能有助于 SHL 疾病的诱导和进展，因此可能被建议作为新的治疗靶点。版权所有 (C) 2010 S. Karger AG，巴塞尔
Even though sudden sensorineural hearing loss (SHL) is a quite frequent disease, the pathogenetic processes leading to it are widely unknown. There is increasing evidence that immunomodulatory cells, especially T lymphocytes, might be involved. Twelve patients with acute SHL and 12 healthy, age-matched individuals were included in this study. In addition to routine blood parameters, plasma levels of tumor necrosis factor alpha (TNF-alpha), soluble CD40 (sCD40) and sCD40 ligand (sCD40L) were determined by ELISA. Moreover, peripheral blood mononuclear cells were isolated by Ficoll density gradient. Afterwards, in subpopulations - identified by CD14 (monocytes), CD68 (macrophages), CD3 (T lymphocytes) or CD19 (B lymphocytes) immunoreactivity - proinflammatory (CD40, TNF-alpha or cyclooxygenase-2) and proadhesive (CD38) proteins were measured by 2-color fluorescence-activated cell sorter analyses. In comparison with healthy individuals, patients with acute SHL revealed elevated plasma levels of sCD40 and sCD40L and a significantly decreased percentage (36%) of lymphocytes, especially of T lymphocytes (28%). Additionally, in patients with acute SHL the percentage of proinflammatory CD40, TNF-alpha, cyclooxygenase-2 or CD38-positive T or B lymphocytes was significantly increased. Our data suggest an enhanced extravasation of proadhesive and proinflammatory lymphocytes from the peripheral circulation, which may contribute to SHL disease induction as well as progression and, thus, may be suggested as a novel therapeutical target. Copyright (C) 2010 S. Karger AG, Basel