Stratton Charles W, Wheldon David B
Department of Pathology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Trends Microbiol. 2006 Nov;14(11):474-9. doi: 10.1016/j.tim.2006.09.002. Epub 2006 Sep 25.
The concept of autoimmune myelinopathy as the primary pathology in multiple sclerosis (MS) is problematic. Vasculitis is seen in the MS brain, both within lesions and in adjacent normal-appearing white matter. The first observation in acute relapse is the sudden, orderly death of oligodendrocytes; inflammatory removal of unsupported myelin seems to be a secondary process. An alternative explanation for these findings is that oligodendrocyte infection might trigger an inflammatory response. Many pathogens, including Chlamydophila (Chlamydia) pneumoniae, have been associated with MS. MS might be an infectious syndrome in which C. pneumoniae has a role in a subset of patients. Mechanisms by which such a cryptic infection could engender relapsing-remitting and, ultimately, progressive disease patterns are discussed.
将自身免疫性髓鞘病视为多发性硬化症(MS)的主要病理学特征这一概念存在问题。在MS患者的大脑中,无论是在病灶内还是在相邻的外观正常的白质中都可见血管炎。急性复发时的首个观察结果是少突胶质细胞突然、有序地死亡;对无支持的髓鞘进行炎症清除似乎是一个次要过程。对这些发现的另一种解释是少突胶质细胞感染可能引发炎症反应。许多病原体,包括肺炎衣原体,都与MS有关。MS可能是一种感染性综合征,其中肺炎衣原体在一部分患者中起作用。本文讨论了这种隐匿性感染引发复发缓解型以及最终进展型疾病模式的机制。