Carlo Contini, Enrico Granieri, Enrico Fainardi, Charles W Stratton
Although the aetiology of Multiple Sclerosis (MS) is unknown, genetic and environmental factors including infectious agents may play a role in the development of this disease. Recent studies have demonstrated chronic cerebrospinal venous insufficiency (CCSVI) as a potential factor in the pathogenesis of clinically defined MS but current evidence does not support a substantial role of CCSVI in the pathogenesis of the classic MS lesions. As the association of Chlamydophila pneumoniae with vascular infections and endothelial dysfunction due to inflammation is well known, C. pneumoniae could be implicated in the development of CCSVI. This hypothesis is based on the ability of this pathogen to infect venous endothelial cells that could contribute to an inflammatory-autoimmune process in venous tissue leading to the venous anomalies (venous stenosis/occlusions) described in CCSVI. In fact, besides the recognized infection by C. pneunoniae of a large variety of cells including alveolar epithelial cells, macrophages, dendritic cells, B and T-cells, neuronal glia and neuronal ependymal cells, this pathogen may also infect vascular endothelial cells in venous tissues. Such an infection/inflammation of venous vascular tissues could contribute to the inflammatory-autoimmune disease causing the venous abnormalities described in the so-called CCSVI.