Charlab R, Blaineau C, Schechtman D, Barcinski M A
Instituto de Biofiscia Carlos Chagas Filho, Universidade Federal do Rio de Janerio, Brazil.
J Protozool. 1990 Sep-Oct;37(5):352-7. doi: 10.1111/j.1550-7408.1990.tb01157.x.
In this paper we show that murine lung conditioned medium (LCM) displays, in addition to its already described colony-stimulating activity on bone marrow cells, a potent growth-stimulating activity on promastigotes of Leishmania mexicana amazonesis. Immunoprecipitation of LCM with an antibody specific for murine granulocyte-macrophage colony stimulating factor (GM-CSF) abrogates both activities, indicating that the leishmanial growth-promoting activity is due to the presence of GM-CSF on LCM. Furthermore, recombinant GM-CSF (rGM-CSF) added to the culture medium or to the immunoprecipitated LCM is able to respectively induce or to partially recover the growth-promoting activity of the LCM. Sequential in vitro passages of the parasite induces a progressive loss of sensitivity to the growth-factor. Parasite forms recently collected from lesions are significantly more responsive to the growth-factor than forms already adapted to grow in culture. Since it has been shown that several different microorganisms display receptors for vertebrate-like hormones and that GM-CSF is able to enhance a cutaneous leishmanial lesion, our results permit us to raise the hypothesis that a direct interaction between a host-derived hormone and a pathogenic microorganism can be of importance in defining the fate of an infection. The fact that GM-CSF is produced by cells that actively participate in a leishmanial infection (T-lymphocytes and macrophages) reinforces our hypothesis.
在本文中，我们表明，鼠肺条件培养基（LCM）除了已描述的对骨髓细胞的集落刺激活性外，对亚马逊利什曼原虫前鞭毛体还具有强大的生长刺激活性。用针对鼠粒细胞-巨噬细胞集落刺激因子（GM-CSF）的特异性抗体对LCM进行免疫沉淀可消除这两种活性，表明利什曼原虫生长促进活性归因于LCM上存在GM-CSF。此外，添加到培养基或免疫沉淀的LCM中的重组GM-CSF（rGM-CSF）能够分别诱导或部分恢复LCM的生长促进活性。寄生虫的连续体外传代导致对生长因子的敏感性逐渐丧失。最近从病变中收集的寄生虫形式比已经适应在培养中生长的形式对生长因子的反应明显更强。由于已经表明几种不同的微生物显示出对脊椎动物样激素的受体，并且GM-CSF能够增强皮肤利什曼原虫病变，我们的结果使我们能够提出这样的假设，即宿主衍生的激素与致病微生物之间的直接相互作用在确定感染的结局中可能很重要。GM-CSF由积极参与利什曼原虫感染的细胞（T淋巴细胞和巨噬细胞）产生这一事实强化了我们的假设。
