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在体内,IgE的产生参与了丁酸盐增强的自然杀伤细胞活性。

IgE production is involved in butyrate-enhanced NK cell activity in vivo.

作者信息

Zhong M, Tai A, Yamamoto I

机构信息

Department of Immunochemistry, Faculty of Pharmaceutical Sciences, Okayama University, Tsushima-naka 1-1-1, Okayama 700-8530, Japan.

出版信息

Chin Med Sci J. 2001 Jun;16(2):76-81.

PMID:12901494
Abstract

It has been demonstrated that patients with asthma have a large number of NK cells and show a stronger NK activity. These results indicate that NK cell activity may be related to total IgE level in serum in healthy subjects. Previously, we have found that sodium butyrate (NaBu) markedly enhanced the IL-4-induced IgE production in the LPS-stimulated murine splenocytes in vitro, and inductive rat IgE production in vivo, and enhanced the NK cell activity ex vivo. We hypothesized that the IgE production might be involved in butyrate-enhanced NK cell activity in vivo. Mice were intraperitoneally treated/immunized with NaBu or/and Ascaris suum extract (ASC), and the spleen NK cell activity was evaluated. Furthermore, the effect of serum (NAS) on IL-2- or IFN-gamma-induced spleen NK cell activity was determined. The spleen NK cell activity and IL-2- or IFN-gamma-induced spleen NK cell activity of mice treated/immunized with NaBu or/and ASC were stronger than those of untreated/unimmunized mice. Although IL-4 blocked IL-2 (100 U/ml)- or IFN-gamma (100 U/ml)-induced increase in NK cell activity, these NK cell activities in mice treated/immunized with NaBu/ASC were not inhibited. IgE production showed a tendency to rise in NaBu-treated mice serum, and a synergistic effect was observed with treatment of NaBu and ASC. Moreover, the NAS significantly increased IL-2(25 U/ml)-or IFN-gamma(25 U/ml)-induced NK cell activity, and its effect was inhibited by anti-mouse IgE mAb. These data show that IgE plays an important role in NAS-enhanced IL-2/IFN-gamma-induced NK cell activity, and IL-4 does not inhibit IgE and IL-2/IFN-gamma-induced NK cell activity in mice.

摘要

已有研究表明,哮喘患者有大量自然杀伤(NK)细胞且表现出更强的NK活性。这些结果表明,NK细胞活性可能与健康受试者血清中的总IgE水平有关。此前,我们发现丁酸钠(NaBu)在体外可显著增强脂多糖(LPS)刺激的小鼠脾细胞中白细胞介素-4(IL-4)诱导的IgE产生,并在体内诱导大鼠IgE产生,且在体外增强NK细胞活性。我们推测,IgE产生可能参与了丁酸钠在体内增强NK细胞活性的过程。用NaBu或/和猪蛔虫提取物(ASC)对小鼠进行腹腔注射/免疫,并评估脾脏NK细胞活性。此外,还测定了血清(NAS)对IL-2或干扰素-γ(IFN-γ)诱导的脾脏NK细胞活性的影响。用NaBu或/和ASC处理/免疫的小鼠的脾脏NK细胞活性以及IL-2或IFN-γ诱导的脾脏NK细胞活性均强于未处理/未免疫的小鼠。尽管IL-4可阻断IL-2(100 U/ml)或IFN-γ(100 U/ml)诱导的NK细胞活性增加,但用NaBu/ASC处理/免疫的小鼠的这些NK细胞活性并未受到抑制。在NaBu处理的小鼠血清中,IgE产生呈上升趋势,且观察到NaBu与ASC联合处理有协同效应。此外,NAS显著增加IL-2(25 U/ml)或IFN-γ(25 U/ml)诱导的NK细胞活性,且其作用可被抗小鼠IgE单克隆抗体抑制。这些数据表明,IgE在NAS增强IL-2/IFN-γ诱导的NK细胞活性中起重要作用,且IL-4不抑制小鼠中IgE和IL-2/IFN-γ诱导的NK细胞活性。

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