Noyori K
Department of Orthopedic Surgery, Yokohama City University School of Medicine, Kanagawa, Japan.
Nihon Seikeigeka Gakkai Zasshi. 1992 May;66(5):525-38.
Sprague Dawley (SD) rats were immunized by subcutaneous injections with heat-killed E. coli 0:14 and lipopolysaccharide (LPS) extracted from E. coli for 15, 29 and 39 weeks which induced arthritis in the ankle. Localization of interleukin-1 (IL-1) and LPS in the ankle joints were investigated immunohistochemically. Serum IgM rheumatoid factor-like substance (RFLS) and anti-LPS IgM were detected by enzyme-linked immunosorbent assay (ELISA). Rats immunized with LPS for 39 weeks developed synovial lining cell hyperplasia in 25 of 40 ankles and lymphoid cell infiltration in 25 and pannus formation in 23, the rates of which were significantly higher than those of control and rats immunized with LPS for 15 and 29 weeks. The induction rate of arthritis in rats immunized with LPS was the same as that in rats immunized with E. coli. LPS and IL-1 were located in synovial cells and pannus in arthritic joints. Changes of RFLS level in rats immunized with LPS were elevated more gradually than those in rats immunized with E. coli. These findings suggest that LPS could stimulate IL-1 and RFLS production and may induce arthritis in rats resembling rheumatoid arthritis.
将斯普拉格-道利(SD)大鼠通过皮下注射热灭活的大肠杆菌0:14和从大肠杆菌中提取的脂多糖(LPS)进行免疫,持续15、29和39周,从而诱发踝关节关节炎。采用免疫组织化学方法研究白细胞介素-1(IL-1)和LPS在踝关节中的定位。通过酶联免疫吸附测定(ELISA)检测血清IgM类风湿因子样物质(RFLS)和抗LPS IgM。用LPS免疫39周的大鼠,40个踝关节中有25个出现滑膜衬里细胞增生,25个出现淋巴细胞浸润,23个出现血管翳形成,其发生率显著高于对照组以及用LPS免疫15周和29周的大鼠。用LPS免疫的大鼠的关节炎诱导率与用大肠杆菌免疫的大鼠相同。LPS和IL-1位于关节炎关节的滑膜细胞和血管翳中。用LPS免疫的大鼠中RFLS水平的变化比用大肠杆菌免疫的大鼠升高得更缓慢。这些发现表明,LPS可刺激IL-1和RFLS的产生,并可能在大鼠中诱发类似类风湿性关节炎的关节炎。