Toivanen P
Department of Medical Microbiology, Turku Immunology Centre, Turku University, Turku, Finland.
J Autoimmun. 2001 May;16(3):369-71. doi: 10.1006/jaut.2000.0496.
Reactive arthritis was initially described as a sterile synovitis, without microbial components present in the joint tissue. It has, however, become evident that bacterial degradation products, and even bacterial DNA, are present in the synovium of patients with this disease. Since intestinal pathogens are important causes of reactive arthritis, and since cellular homing allows transport of bacterial products from the gut to synovium, we have approached the etiology of rheumatoid arthritis from this point of view. A series of observations has led to a hypothesis that patients with rheumatoid arthritis might favour, for genetic reasons, intestinal bacteria which are capable of inducing arthritis. In the long-run, with continuous seeding of bacterial products from the gut, the synovial inflammation is followed by erosion, exposition of cartilage antigens, and autoimmunity.
反应性关节炎最初被描述为一种无菌性滑膜炎,关节组织中不存在微生物成分。然而,现已明确,在患有这种疾病的患者滑膜中存在细菌降解产物,甚至细菌DNA。由于肠道病原体是反应性关节炎的重要病因,且细胞归巢可使细菌产物从肠道转运至滑膜,我们从这一角度探讨了类风湿性关节炎的病因。一系列观察结果引发了一种假说,即类风湿性关节炎患者可能由于遗传原因,更倾向于携带能够诱发关节炎的肠道细菌。从长远来看,随着肠道细菌产物的持续植入,滑膜炎症会继而引发侵蚀、软骨抗原暴露及自身免疫反应。