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从一种寄生虫中分离出的巨噬细胞移动抑制因子可抑制特应性哮喘患者外周血单核细胞中Th2细胞因子的产生。

Macrophage migration inhibitory factor isolated from a parasite inhibited Th2 cytokine production in PBMCs of atopic asthma patients.

作者信息

Park Hye-Kyung, Cho Min Kyoung, Park Hee Young, Kim Ki Uk, Kim Yun Seong, Lee Min Ki, Park Soon Kew, Kim Dong-Hee, Yu Hak Sun

机构信息

Department of Internal Medicine, School of Medicine, Pusan National University, Busan, Republic of Korea.

出版信息

J Asthma. 2012 Feb;49(1):10-5. doi: 10.3109/02770903.2011.637593. Epub 2011 Dec 7.

Abstract

BACKGROUND

In a previous study, we demonstrated that the human macrophage migration inhibitory factor (MIF)-like protein (As-MIF) isolated from helminths could inhibit allergic airway inflammation via the recruitment of CD4(+)CD25(+)Foxp3(+) T cells.

OBJECTIVE

To evaluate the clinical importance of As-MIF as an antiasthma drug, we evaluated immune responses after recombinant As-MIF (rAs-MIF) treatment in peripheral blood mononuclear cell (PBMC) cultures.

METHODS

PBMC was isolated from 10 patients with atopic asthma, 8 patients with nonatopic asthma, and 12 nonatopic healthy subjects, and various concentrations of rAs-MIF were transferred into the PBMC culture medium. After 3 days, we measured the levels of T helper 2 and T helper 1 cytokines via ELISA.

RESULTS

In atopic asthma, IL-4 and IL-5 production was significantly reduced in the PBMC cultures after rAs-MIF treatment. These inhibitory effects were not observed in the nonatopic asthma group. By way of contrast, IL-10 production in the PMBC cultures was significantly increased after rAs-MIF treatment in all experimental groups.

CONCLUSION

The results of this study are similar to those previously reported in a mouse study, suggesting that As-MIF might be a candidate for the specific treatment of asthma.

摘要

背景

在之前的一项研究中,我们证明从蠕虫中分离出的人类巨噬细胞移动抑制因子(MIF)样蛋白(As-MIF)可通过募集CD4(+)CD25(+)Foxp3(+) T细胞来抑制过敏性气道炎症。

目的

为评估As-MIF作为一种抗哮喘药物的临床重要性,我们在人外周血单个核细胞(PBMC)培养物中评估了重组As-MIF(rAs-MIF)治疗后的免疫反应。

方法

从10例特应性哮喘患者、8例非特应性哮喘患者和12例非特应性健康受试者中分离出PBMC,并将不同浓度的rAs-MIF加入PBMC培养基中。3天后,我们通过酶联免疫吸附测定法检测辅助性T细胞2和辅助性T细胞1细胞因子的水平。

结果

在特应性哮喘患者中,rAs-MIF治疗后PBMC培养物中白细胞介素-4(IL-4)和白细胞介素-5(IL-5)的产生显著减少。在非特应性哮喘组中未观察到这些抑制作用。相比之下,在所有实验组中,rAs-MIF治疗后PBMC培养物中白细胞介素-10(IL-10)的产生显著增加。

结论

本研究结果与先前在小鼠研究中报道的结果相似,提示As-MIF可能是哮喘特异性治疗的候选药物。

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