Mason P R, Gwanzura L
Department of Medical Microbiology, University of Zimbabwe Medical School, Harare.
Infect Immun. 1990 Nov;58(11):3553-7. doi: 10.1128/iai.58.11.3553-3557.1990.
Proliferative responses to mitogens were determined by using peripheral blood mononuclear cells from women with active trichomoniasis, with serological evidence of past infection with Trichomonas vaginalis, and with no evidence of current or past infection. Even after the human immunodeficiency virus antibody status of the patients was taken into account, cells from women with active trichomoniasis showed reduced responses to phytohemagglutinin, concanavalin A, pokeweed mitogen, and bacterial lipopolysaccharide. Similar findings were obtained by using spleen cells from mice inoculated subcutaneously with live trichomonads. Reduction in proliferative responses by these cells could be detected 3 days after inoculation. There was some evidence to suggest that more-pathogenic strains of the parasite induced a greater degree of immunosuppression. The responses of spleen cells from mice inoculated with trichomonad-free culture supernatants were within normal limits, indicating that live trichomonads were needed to induce suppression. Support for this was gained from studies with cells from women who were treated successfully. Cells from these women rapidly regained normal lymphoproliferative function. Interleukin-2 (IL-2) production by spleen cells from infected mice was determined from measurements of mitochondrial activity in an IL-2-dependent T-cell line following incubation with stimulated spleen cell culture supernatants. These tests demonstrated lower IL-2 activity in supernatants from cell cultures from infected mice than in those from uninfected mice. The reduction in IL-2 activity did not, however, appear to correlate with the degree of reduction of mitogen-induced lymphoproliferation. Suppression of T-cell-mediated immunity may be one of the mechanisms by which T. vaginalis is able to evade host responses to infection.
通过使用来自患有活动性滴虫病的女性、有阴道毛滴虫既往感染血清学证据的女性以及无当前或既往感染证据的女性的外周血单个核细胞,来测定对有丝分裂原的增殖反应。即使考虑了患者的人类免疫缺陷病毒抗体状态,患有活动性滴虫病的女性的细胞对植物血凝素、刀豆球蛋白A、商陆有丝分裂原和细菌脂多糖的反应仍降低。通过使用皮下接种活滴虫的小鼠的脾细胞也获得了类似的结果。接种后3天即可检测到这些细胞增殖反应的降低。有证据表明,寄生虫的致病性更强的菌株会诱导更大程度的免疫抑制。接种无滴虫培养上清液的小鼠的脾细胞反应在正常范围内,这表明需要活滴虫来诱导抑制作用。对成功接受治疗的女性的细胞进行的研究也支持了这一点。这些女性的细胞迅速恢复了正常的淋巴细胞增殖功能。通过在与刺激的脾细胞培养上清液孵育后,测定IL-2依赖的T细胞系中的线粒体活性,来确定感染小鼠的脾细胞产生白细胞介素-2(IL-2)的情况。这些试验表明,感染小鼠的细胞培养上清液中的IL-2活性低于未感染小鼠的上清液。然而,IL-2活性的降低似乎与有丝分裂原诱导的淋巴细胞增殖的降低程度无关。T细胞介导的免疫抑制可能是阴道毛滴虫逃避宿主感染反应的机制之一。