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肝硬化和肝细胞癌患者经脂多糖刺激的单核细胞培养上清液中白细胞介素1活性降低。

Decreased interleukin 1 activity in culture supernatant of lipopolysaccharide stimulated monocytes from patients with liver cirrhosis and hepatocellular carcinoma.

作者信息

Yokota M, Sakamoto S, Koga S, Ibayashi H

出版信息

Clin Exp Immunol. 1987 Feb;67(2):335-42.

Abstract

Immunoregulatory function of peripheral blood monocytes was studied in patients with hepatocellular carcinoma (HCC) and liver cirrhosis (LC), by assaying interleukin 1 (IL-1) and prostaglandin E2 (PGE2) in the culture supernatant of lipopolysaccharide-stimulated monocytes. IL-1 activity of the monocyte culture supernatant without indomethacin was decreased in patients with HCC and LC, compared with that of controls. The activity was lower in patients with HCC than that in those with LC. The PGE2 content of the culture supernatant of monocytes from patients with LC and HCC was increased, compared to normal controls. To avoid the effect of PGE2 on the IL-1 assay, we cultured the monocytes with addition of indomethacin and assayed IL-1 activity in the culture supernatant. As a result, monocyte IL-1 production was increased in patients with HCC and LC, compared with normal controls. The decrease in IL-1 activity of the supernatant without indomethacin of patients with LC and HCC was considered to be due to increased secretion of PGE2 by the monocytes. Therefore, monocytes from patients with HCC and LC had an increased capacity of secreting both IL-1 and PGE2 over normal controls, but the effect of the suppressor function (PGE2 secretion) dominated in these patients.

摘要

通过检测脂多糖刺激的单核细胞培养上清液中的白细胞介素1(IL-1)和前列腺素E2(PGE2),研究了肝细胞癌(HCC)和肝硬化(LC)患者外周血单核细胞的免疫调节功能。与对照组相比,未使用吲哚美辛的HCC和LC患者单核细胞培养上清液的IL-1活性降低。HCC患者的活性低于LC患者。与正常对照组相比,LC和HCC患者单核细胞培养上清液中的PGE2含量增加。为避免PGE2对IL-1检测的影响,我们在培养单核细胞时添加吲哚美辛,并检测培养上清液中的IL-1活性。结果,与正常对照组相比,HCC和LC患者的单核细胞IL-1产生增加。LC和HCC患者未使用吲哚美辛的上清液中IL-1活性降低被认为是由于单核细胞分泌PGE2增加所致。因此,与正常对照组相比,HCC和LC患者的单核细胞分泌IL-1和PGE2的能力增强,但在这些患者中抑制功能(PGE2分泌)的作用占主导。

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Impaired monocyte function in liver cirrhosis.肝硬化患者单核细胞功能受损。
Br Med J (Clin Res Ed). 1981 Apr 18;282(6272):1262-3. doi: 10.1136/bmj.282.6272.1262.

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