Mayatepek E, Flock B, Zelezny R, Kreutzer K, von Giesen H J
Department of General Pediatrics, University Children's Hospital, 69120 Heidelberg, Germany.
J Infect Dis. 1999 Mar;179(3):714-6. doi: 10.1086/314619.
Previous studies on macrophages have shown that Toxoplasma gondii alters the metabolism of arachidonic acid with subsequent inability to generate leukotrienes (LT)s. LTB4 and LTC4 were analyzed in cerebrospinal fluid of 3 groups of human immunodeficiency virus (HIV) type 1-seropositive patients: with toxoplasmic encephalitis (TE) (n=10), with herpes simplex encephalitis (n=5), and without encephalitis (n=10) and in HIV-1-seronegative controls without inflammatory diseases (n=30) by specific immunoassays and gas chromatography-mass spectrometry. In HIV-1-seropositive subjects with TE, LTB4 and LTC4 were below the detection limit (<5.0 pg/mL) and thus significantly decreased (P<.01) compared with HIV-1-seropositive patients with herpes simplex encephalitis (LTB4, 148.5+/-47.6 pg/mL; LTC4, 116.4+/-36.9 pg/mL) and in those without encephalitis (LTB4, 46.1+/-16.8 pg/mL; LTC4, 48.3+/-21.3 pg/mL), and in controls (LTB4, 43.6+/-21.2; LTC4, 45.2+/-18.9 pg/mL). These results point to an essential role of inhibition of 5-lipoxygenase with subsequent failure of LT release as an important mechanism for the survival of T. gondii in vivo.
先前对巨噬细胞的研究表明，弓形虫会改变花生四烯酸的代谢，随后无法生成白三烯（LT）。通过特异性免疫测定和气相色谱-质谱分析法，对三组1型人类免疫缺陷病毒（HIV）血清阳性患者的脑脊液中的LTB4和LTC4进行了分析：患有弓形虫性脑炎（TE）的患者（n = 10）、患有单纯疱疹性脑炎的患者（n = 5）、未患脑炎的患者（n = 10），以及无炎症性疾病的HIV-1血清阴性对照者（n = 30）。在患有TE的HIV-1血清阳性受试者中，LTB4和LTC4低于检测限（<5.0 pg/mL），因此与患有单纯疱疹性脑炎的HIV-1血清阳性患者（LTB4，148.5±47.6 pg/mL；LTC4，116.4±36.9 pg/mL）、未患脑炎的患者（LTB4，46.1±16.8 pg/mL；LTC4，48.3±21.3 pg/mL）以及对照者（LTB4，43.6±21.2；LTC4，45.2±18.9 pg/mL）相比，显著降低（P<0.01）。这些结果表明，抑制5-脂氧合酶并随后导致LT释放失败，在弓形虫在体内存活的重要机制中起着至关重要的作用。
