Skaleric U, Allen J B, Smith P D, Mergenhagen S E, Wahl S M
Laboratory of Immunology, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892.
J Immunol. 1991 Oct 15;147(8):2559-64.
Peritoneal and peripheral blood monocyte-macrophages from inbred Lewis (LEW) rats generate higher levels of reactive oxygen intermediates (ROI) in response to group A streptococcal cell walls (SCW) than do similar populations of cells from histocompatible Fischer rats. This differential sensitivity of the phagocytes to SCW is reflected in differences in susceptibility of the two strains to the development of arthritis in response to SCW. After systemic administration of the SCW, LEW rats develop acute and chronic erosive polyarthritis, whereas the Fischer rats are arthritis resistant. Inasmuch as these data suggested that the SCW-induced release of inflammatory cell products such as ROI might be an important contributory factor in the pathogenesis of arthritis in the LEW rats, the animals were injected with SCW and treated with ROI inhibitors. A single intraarticular injection of superoxide dismutase or catalase significantly reduced the SCW-induced inflammatory response and evolution of erosive arthritis in the treated animals (articular index 3.6 +/- 0.36 for SCW only vs 1.4 +/- 0.3 for SCW + SOD; p less than 0.001; n = 6). These data indicate that ROI play a pivotal role in synovitis and, furthermore, that suppression of these inflammatory mediators modulates both acute and chronic SCW-induced inflammation of the joint.
与组织相容性的Fischer大鼠的相似细胞群体相比，近交系Lewis（LEW）大鼠的腹膜和外周血单核细胞 - 巨噬细胞对A组链球菌细胞壁（SCW）产生更高水平的活性氧中间体（ROI）。吞噬细胞对SCW的这种差异敏感性反映在两种品系对SCW诱导的关节炎发展的易感性差异上。全身给予SCW后，LEW大鼠发展为急性和慢性侵蚀性多关节炎，而Fischer大鼠对关节炎有抗性。鉴于这些数据表明SCW诱导的炎症细胞产物如ROI的释放可能是LEW大鼠关节炎发病机制中的一个重要促成因素，给动物注射SCW并用ROI抑制剂进行治疗。单次关节内注射超氧化物歧化酶或过氧化氢酶可显著降低治疗动物中SCW诱导的炎症反应和侵蚀性关节炎的进展（仅SCW组的关节指数为3.6±0.36，而SCW + SOD组为1.4±0.3；p<0.001；n = 6）。这些数据表明ROI在滑膜炎中起关键作用，此外，抑制这些炎症介质可调节SCW诱导的关节急性和慢性炎症。
