Tuomanen E, Hengstler B, Rich R, Bray M A, Zak O, Tomasz A
J Infect Dis. 1987 May;155(5):985-90. doi: 10.1093/infdis/155.5.985.
An increased inflammatory mass in the subarachnoid space during bacterial meningitis may correlate with a poor outcome of disease. Using a rabbit model of pneumococcal meningitis, we sought to reduce this inflammatory process. The ability of the pneumococcal cell wall to cause death and to generate leukocytosis and abnormal chemistry in cerebrospinal fluid was prevented when animals were treated with inhibitors of cyclooxygenase pathway of arachidonate metabolism. Bacterial lysis by ampicillin led to release of cell wall that caused a significant, transient increase in meningeal inflammation. This inflammatory burst was also prevented by administering cyclooxygenase inhibitors concurrently with the antibiotic.
细菌性脑膜炎期间蛛网膜下腔炎症性肿块增加可能与疾病的不良预后相关。我们使用肺炎球菌性脑膜炎兔模型,试图减轻这一炎症过程。当用花生四烯酸代谢的环氧化酶途径抑制剂治疗动物时,肺炎球菌细胞壁导致死亡、引起脑脊液中白细胞增多和化学指标异常的能力受到抑制。氨苄青霉素引起的细菌裂解导致细胞壁释放,从而引起脑膜炎症显著短暂增加。同时给予环氧化酶抑制剂和抗生素也可防止这种炎症爆发。