Delemarre F G, Stevenhagen A, Kroon F P, van Furth R
Department of Infectious Diseases, University Hospital, Leiden, The Netherlands.
Scand J Immunol. 1998 Feb;47(2):163-6.
In the present study the role of granulocyte-macrophage colony stimulating factor (GM-CSF) in the reduced toxoplasmastatic activity of monocytes was investigated in patients with acquired immunodeficiency syndrome (AIDS). The secretion of GM-CSF by non-stimulated monocytes and by Toxoplasma gondii-infected monocytes from AIDS patients did not differ from that of healthy individuals. Furthermore, GM-CSF was not detected in sera from AIDS patients and healthy individuals. However, upon stimulation with lipopolysaccharide (LPS), monocytes from AIDS patients released significantly more GM-CSF than those from healthy individuals. Incubation of monocytes from AIDS patients with polyclonal antibodies against GM-CSF restored their inhibitory activity against T. gondii. On the basis of the present and earlier results the putative mechanism of reduced toxoplasmastatic activity of monocytes from AIDS patients may be as follows: upon stimulation with human immunodeficiency virus (HIV) the increased synthesis of GM-CSF by monocytes stimulates the production of prostaglandin E2 (PGE2) which, in turn, impairs the toxoplasmastatic activity of these cells.
在本研究中,对获得性免疫缺陷综合征(AIDS)患者体内粒细胞巨噬细胞集落刺激因子(GM-CSF)在单核细胞弓形虫抑制活性降低中所起的作用进行了研究。AIDS患者未受刺激的单核细胞以及受刚地弓形虫感染的单核细胞分泌GM-CSF的情况与健康个体并无差异。此外,在AIDS患者和健康个体的血清中均未检测到GM-CSF。然而,在用脂多糖(LPS)刺激后,AIDS患者的单核细胞释放的GM-CSF明显多于健康个体。用抗GM-CSF的多克隆抗体孵育AIDS患者的单核细胞可恢复其对刚地弓形虫的抑制活性。基于目前及早期的研究结果,AIDS患者单核细胞弓形虫抑制活性降低的可能机制如下:在受到人类免疫缺陷病毒(HIV)刺激后,单核细胞GM-CSF合成增加,刺激前列腺素E2(PGE2)的产生,而PGE2反过来又损害这些细胞的弓形虫抑制活性。