摘要
目的研究细菌脂多糖对小鼠巨噬细胞的生长调节作用。方法应用小鼠腹腔渗出性巨噬细胞(PEM)和巨噬细胞株J774A.1为靶细胞,测定细菌脂多糖(LPS)对M-CSF和GM-CSF刺激的巨噬细胞集落细胞形成的影响,同时用125Ⅰ标记的GM-CSF受体结合实验测定了LPS对巨噬细胞膜上的GM-CSF受体数目的调节。用反向PCR(RT-PCR)法检测TTGF-β1对巨噬细胞产生IFN-γ的作用。结果LPS单独对巨噬细胞无生长调节作用,但可抑制GM-CSF对巨噬细胞的增殖效应。而在TGF-β1同时存在下,LPS的抑制效应被消除。RT-PCR证实LPS诱生巨噬细胞产生的IFN-γ可被TGF-β1有效地抑制.而已知IFN-γ是强烈的巨噬细胞生长抑制因子。此外,125Ⅰ-GM-CSF受体结合实验发现,同TGF-β1一样LPS增强GM-CSF受体数目的表达。结论LPS参与了多种细胞因子对巨噬细胞生长的调节网络,根据存在的细胞因子不同,表现为抑制和增殖的双重作用。
To study bacterial lipopolysaccharide(LPS) effects on murine macrophage proliferation, Methods Murine peritoneal exudate macrophage (PEM) and macrophage cell line J_(774)A. 1 as target, LPS effects on M-CSF and GM-CSF stimulated macrophage colony-forming Cells(CFU-M)were employed. ̄(125)Ⅰ-GM-CSF receptor binding assay was used to examine LPS regulation on GMCSF receptor expression。 RT-PCR was developed to test TGF-β1, inhabitation of IFN-γmRNA expression on macrophage induced by LPS. ResuIts In spite of no direct effect on macrophage proliferation, LPS could inhibit the macrophage proliferation stimulated by granulocyte-macrophage colony-stimulating factor(GM-CSF). However, under the concomitant existence of GM-CSF and TGF-β1, the LPS inhibitory effect was deprived. RT-PCR analysis indicated that the strongest macrophage growth inhibitory factor IFN-γmRNA expression in macrophage induced by LPS was remarkably suppressed by TGF-β1. ̄(125)Ⅰ-GM-CSF receptor binding assay found that LPS could enhance GMCSF receptor expression as similar as TGF-β1. Conclusions All the resuIts imply that LPS involves in the network of macrophage proliferative regulation by muItiple cytokines displaying inhibitory and stimulatOfy effects dependent on co-existing cytokines.
出处
《中华肝脏病杂志》
CAS
CSCD
1996年第2期94-96,共3页
Chinese Journal of Hepatology
关键词
细菌脂多糖
巨噬细胞
生长调节
Lipopolysaccharide macrophage Growth regulator