Anguita Juan, Samanta Swapna, Ananthanarayanan Shobana K, Revilla Beatriz, Geba Gregory P, Barthold Stephen W, Fikrig Erol
Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
FEMS Immunol Med Microbiol. 2002 Nov 15;34(3):187-91. doi: 10.1111/j.1574-695X.2002.tb00623.x.
Cyclooxygenase (Cox) is a key enzyme in the biosynthetic metabolism of prostaglandins. The inducible isoform of Cox-2 has been implicated in inflammation and its specific inhibition can be used to treat noninfectious inflammatory diseases, such as rheumatoid arthritis. Borrelia burgdorferi, the agent of Lyme disease, can induce joint inflammation. Here we show that B. burgdorferi induced the upregulation of cox-2 gene expression in murine joints at the onset of arthritis in infected mice. The level of mRNA expression correlated with the degree of inflammation. The specific inhibition of Cox-2 diminished the degree of joint inflammation, without affecting B. burgdorferi-specific antibody or cytokine responses. Cox-2 activity is therefore associated with the genesis of infectious arthritis caused by B. burgdorferi.
环氧化酶（Cox）是前列腺素生物合成代谢中的关键酶。Cox-2的诱导型同工酶与炎症有关，其特异性抑制可用于治疗非感染性炎症性疾病，如类风湿性关节炎。莱姆病的病原体伯氏疏螺旋体可诱发关节炎症。在此我们表明，在感染小鼠关节炎发作时，伯氏疏螺旋体可诱导小鼠关节中cox-2基因表达上调。mRNA表达水平与炎症程度相关。Cox-2的特异性抑制降低了关节炎症程度，而不影响针对伯氏疏螺旋体的抗体或细胞因子反应。因此，Cox-2活性与伯氏疏螺旋体引起的感染性关节炎的发生有关。
