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血清巨噬细胞移动抑制因子作为活动性肺结核的生物标志物。

Serum Macrophage Migration Inhibitory Factor as a Biomarker of Active Pulmonary Tuberculosis.

机构信息

Department of Clinical Laboratory, Wuxi Huishan People's Hospital, Wuxi, Jiangsu, China.

Department of Clinical Laboratory, The Fifth People's Hospital of Wuxi, Affiliated to Jiangnan University, Wuxi, Jiangsu, China.

出版信息

Ann Lab Med. 2018 Jan;38(1):9-16. doi: 10.3343/alm.2018.38.1.9.

DOI:10.3343/alm.2018.38.1.9
PMID:29071813
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5700157/
Abstract

BACKGROUND

Macrophage migration inhibitory factor (MIF), a pro-inflammatory cytokine with chemokine-like functions, has been shown to play a central role in several acute and chronic inflammatory diseases. However, limited information is available regarding the use of MIF as an inflammatory pathway marker in patients with tuberculosis. This study aimed to investigate the association of MIF with IFN-γ and TNF-α in active pulmonary tuberculosis (APTB) following anti-tuberculosis treatment.

METHODS

The MIF, TNF-α, and IFN-γ serum levels were determined in 47 patients with APTB by cytokine-specific ELISA at four phases: prior to anti-tuberculosis drug treatment (baseline), and following 2, 4, and 6 months of treatment. In addition, we measured the MIF, TNF-α, and IFN-γ serum levels in 50 health controls.

RESULTS

MIF serum levels were significantly elevated (P<0.05) in patients with APTB prior to treatment compared with that in control subjects, and TNF-α ≥449.7 pg/mL was associated with high MIF levels (≥13.1 ng/mL). MIF levels were significantly reduced (P<0.01) following 2, 4, and 6 months of treatment, with variations in TNF-α and IFN-γ serum levels. MIF levels were positively correlated with the paired TNF-α level at baseline (r=0.1103, P=0.0316) and following 6 months of treatment (r=0.09569, P=0.0364).

CONCLUSIONS

A reduction in the MIF serum levels in patients with APTB following anti-tuberculosis treatment may positively affect host immune protection against Mycobacterium tuberculosis infection. Thus, serum MIF levels may constitute a useful marker for assessing therapy effectiveness in patients with APTB.

摘要

背景

巨噬细胞移动抑制因子(MIF)是一种具有趋化因子样功能的促炎细胞因子,已被证明在几种急性和慢性炎症性疾病中发挥核心作用。然而,关于 MIF 作为结核患者炎症途径标志物的应用,信息有限。本研究旨在探讨 MIF 与 IFN-γ 和 TNF-α 在抗结核治疗后活动性肺结核(APTB)中的相关性。

方法

采用细胞因子特异性 ELISA 法检测 47 例 APTB 患者在抗结核药物治疗前(基线)和治疗后 2、4、6 个月的 MIF、TNF-α 和 IFN-γ 血清水平。此外,我们还测量了 50 名健康对照者的 MIF、TNF-α 和 IFN-γ 血清水平。

结果

治疗前 APTB 患者的 MIF 血清水平显著升高(P<0.05),与对照组相比,TNF-α≥449.7pg/ml 与高 MIF 水平(≥13.1ng/ml)相关。治疗后 2、4 和 6 个月时,MIF 水平显著降低(P<0.01),TNF-α和 IFN-γ 血清水平也随之变化。MIF 水平与基线时配对 TNF-α水平呈正相关(r=0.1103,P=0.0316),与治疗后 6 个月时的 TNF-α水平呈正相关(r=0.09569,P=0.0364)。

结论

抗结核治疗后 APTB 患者的 MIF 血清水平降低可能对宿主免疫保护对抗结核分枝杆菌感染产生积极影响。因此,血清 MIF 水平可能成为评估 APTB 患者治疗效果的有用标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d734/5700157/94595d869100/alm-38-9-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d734/5700157/a4545a72891f/alm-38-9-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d734/5700157/bd0f1419622b/alm-38-9-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d734/5700157/94595d869100/alm-38-9-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d734/5700157/a4545a72891f/alm-38-9-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d734/5700157/bd0f1419622b/alm-38-9-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d734/5700157/94595d869100/alm-38-9-g003.jpg

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Pro-inflammatory action of MIF in acute myocardial infarction via activation of peripheral blood mononuclear cells.MIF 在急性心肌梗死中的促炎作用是通过激活外周血单核细胞实现的。
PLoS One. 2013 Oct 1;8(10):e76206. doi: 10.1371/journal.pone.0076206. eCollection 2013.
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Arrest Functions of the MIF Ligand/Receptor Axes in Atherogenesis.
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