Bersudsky M, Apte R N, El-On J
Department of Microbiology and Immunology, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, 84105, Israel.
Exp Parasitol. 2000 Mar;94(3):150-7. doi: 10.1006/expr.1999.4486.
In this study, the pattern of interleukin-1alpha (IL-1alpha) production by both peritoneal (PM) and bone marrow macrophages (BMM) from resistant (C3H/HeJ) and susceptible (BALB/c) mice was investigated, using a bioassay and an IL-1alpha-specific ELISA kit. PM from normal uninfected mice showed either an initial high (C3H/HeJ) or a neglected (BALB/c) level of IL-1alpha activity, respectively, probably due to thioglycollate stimulation. Infection with Leishmania major induced only a marginal effect on IL-1 production by both cells. Normal, uninfected and unstimulated BMM from both mice did not produce IL-1alpha over a 7-day period of cultivation in vitro. Upon stimulation with either lipopolysaccharide (LPS) (BALB/c) or concanavalin A (Con A) (C3H/HeJ), both cell types produced IL-1alpha that peaked within the first 12-24 h following stimulation. BMM from C3H/HeJ and BALB/c mice failed to produce IL-1alpha when infected in vitro with L. major or L. donovani promastigotes. However, infection with these two parasites did not interfere with the capability of the host cell to produce IL-1alpha when stimulated with LPS or Con A. The level of IL-1alpha production was independent of the degree of parasitization of the macrophages. Similar results were observed with IL-1beta and IL-6 production by BMM, even though their levels were generally slightly higher than those obtained with IL-1alpha.
在本研究中，使用生物测定法和白细胞介素-1α（IL-1α）特异性酶联免疫吸附测定试剂盒，研究了抗性（C3H/HeJ）和易感（BALB/c）小鼠的腹腔巨噬细胞（PM）和骨髓巨噬细胞（BMM）产生IL-1α的模式。来自正常未感染小鼠的PM分别显示出初始高水平（C3H/HeJ）或被忽视的水平（BALB/c）的IL-1α活性，这可能是由于巯基乙酸盐刺激所致。感染硕大利什曼原虫对两种细胞产生IL-1的影响仅微乎其微。来自两种小鼠的正常、未感染且未受刺激的BMM在体外培养7天期间均未产生IL-1α。在用脂多糖（LPS）（BALB/c）或伴刀豆球蛋白A（Con A）（C3H/HeJ）刺激后，两种细胞类型均产生IL-1α，其在刺激后的最初12 - 24小时内达到峰值。当在体外感染硕大利什曼原虫或杜氏利什曼原虫前鞭毛体时，来自C3H/HeJ和BALB/c小鼠的BMM无法产生IL-1α。然而，当用LPS或Con A刺激时，感染这两种寄生虫并未干扰宿主细胞产生IL-1α的能力。IL-1α的产生水平与巨噬细胞的寄生程度无关。在用BMM产生IL-1β和IL-6方面也观察到了类似结果，尽管它们的水平通常略高于用IL-1α获得的水平。
