Analysis of interleukin 6 and its soluble receptor in cerebrospinal fluid

在去年的报告中，我们提出胶质母细胞瘤细胞系T98G在感染1型疱疹病毒（HSV1）时产生白细胞介素6 （IL6）。随后的实验表明，诱导il - 6产生的不是HSV感染本身，而是病毒制备过程中被污染的某种因子。低浓度脂多糖（LPS）对T98G产生IL6没有促进作用，但LPS刺激的外周血单核细胞（PBM）培养上清具有较强的IL6诱导活性。我们可以证明，低剂量LPS刺激的多形核细胞（PMN）上清液也具有相同的活性。此外，我们可以认为，在PMN的情况下，IL1以外的某些因子可能对IL6的诱导活性起主要作用，而在PBM的情况下，IL1可能很重要。星形细胞瘤细胞系U373也获得了相同的结果。有趣的是，最初可能出现在炎症部位的PMN参与了IL6产生的调节。我们正在研究感染或未感染HSV1的U373细胞中IL6信息水平的变化。脑脊液中存在的免疫反应性可溶性il - 6受体（sIL6R）具有生物活性。因此，我们推测CSF中的sIL6R可能存在于IL6-sIL6R复合物中。令人惊讶的是，当将csf应用于凝胶过滤并测定每个馏分中的IL6和sIL6R时，没有观察到il - 6-sIL6R复合物的峰值。这可能表明只有一小部分sIL6R与IL6结合，其余的sIL6R和IL6以自由形式存在。

In the report last year, we suggested that glioblastoma cell line T98G produce interleukin 6 (IL6) when it was infected with herpes virus type 1 (HSV1). Subsequent experiment revealed that it is not HSV infection itself but some factor contaminated in the virus preparation that induce IL6 production. Lipopolysaccharide (LPS) in low concentration dose not enhance IL6 production from T98G,but the supernatant of LPS stimulated peripheral blood mononuclear cells (PBM) culture has strong IL6 inducing activity. We could demonstrate that the supernatants of low dose LPS stimulated polymorphonuclear cell (PMN) also have the same activity. Furthermore, we could suggest that in case of PMN some factor other than IL1 may play major role for IL6 inducing activity, while IL1 may be important in case of PBM.The same results were obtained using astrocytoma cell line U373. It is interesting that PMN that may appear at inflammatory site at first are involved for the regulation of IL6 production. The change of IL6 message level in U373 cells with or without HSV1 infection is under investigation.The immunoreactive soluble IL6 receptor (sIL6R) present in cerebrospinal fluid is shown to biologically active. Thus, we speculated that sIL6R in CSF may be present in IL6-sIL6R complex. Surprisingly, when CSFs were applied to gel filtration and IL6 and sIL6R in each fraction were assayd, no peak suggesting IL6-sIL6R complex was observed. This may suggest that only a small part of sIL6R bind to IL6 and rest of sIL6R and IL6 is present in free form.