Abou-Donia Mohamed Bahie, Lieberman Allan, Curtis Luke
1 Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC, USA.
2 Center for Occupational and Environmental Medicine, North Charleston, SC, USA.
Toxicol Ind Health. 2018 Jan;34(1):44-53. doi: 10.1177/0748233717733852. Epub 2017 Oct 25.
A number of studies have linked exposures to industrial and household chemicals and biological toxins to increased risk of autoimmunity in general and elevated levels of autoantibodies to neural antigens specifically. Elevated neural autoantibodies are biomarkers for many diseases such as multiple sclerosis and Parkinson's disease. Our study reports levels of six types of neural autoantibodies in a group of 24 toxicant-exposed patients. The patients were exposed to a variety of toxicants including contaminated drinking water (four patients), building water/mold damage (eight patients), pesticides (four patients), and other assorted toxic chemicals (eight patients). Levels of all six neural autoantibodies were significantly elevated in most patients and in the patient group at large, with mean antibody levels for the 24 chemically exposed patients (relative to a healthy control population), in descending order: 475% for tau proteins, 391% for microtubule associated proteins-2, 334% for neurofilament proteins (NFP), 302% for myelin basic protein, 299% for glial fibrillary acidic proteins, and 225% for tubulin. Tau protein autoantibodies were significantly elevated in the patient groups with peripheral neuropathy, muscle and joint pain, asthma, and chemical sensitivity. Autoantibodies to tubulin were significantly higher in the chemical sensitivity and asthma patients, autoantibodies to NFP were significantly higher in the patients with sleep apnea, whereas S-100B autoantibodies were significantly increased in patients with muscle/joint pain, asthma, and apnea/insomnia. In patients exposed to environmental toxicants, measurements of autoantibodies may be useful for prevention, diagnosis, and treatment. This study adds to the scientific literature the ability of a broad spectrum of environmental triggers adversely affecting the nervous system through the process of autoimmunity, which may explain the increasing incidence of neurodegenerative diseases.
多项研究表明，接触工业和家用化学品以及生物毒素会增加自身免疫的总体风险，特别是会提高针对神经抗原的自身抗体水平。高水平的神经自身抗体是许多疾病的生物标志物，如多发性硬化症和帕金森病。我们的研究报告了一组24名接触毒物患者体内六种神经自身抗体的水平。这些患者接触了多种毒物，包括受污染的饮用水（4名患者）、建筑用水/霉菌损害（8名患者）、农药（4名患者）以及其他各类有毒化学物质（8名患者）。大多数患者以及整个患者群体中，所有六种神经自身抗体的水平均显著升高。24名化学物质接触患者的平均抗体水平（相对于健康对照人群），从高到低依次为：tau蛋白475%、微管相关蛋白-2 391%、神经丝蛋白（NFP）334%、髓鞘碱性蛋白302%、胶质纤维酸性蛋白299%、微管蛋白225%。tau蛋白自身抗体在患有周围神经病变、肌肉和关节疼痛、哮喘以及化学敏感性的患者群体中显著升高。微管蛋白自身抗体在化学敏感性和哮喘患者中显著更高，NFP自身抗体在睡眠呼吸暂停患者中显著更高，而S-100B自身抗体在肌肉/关节疼痛、哮喘以及呼吸暂停/失眠患者中显著升高。对于接触环境毒物的患者，检测自身抗体可能有助于预防、诊断和治疗。这项研究为科学文献增添了内容，表明广泛的环境触发因素可通过自身免疫过程对神经系统产生不利影响，这可能解释了神经退行性疾病发病率不断上升的原因。
