Analysis of macrophage migration inhibitory factor (MIF) in patients with idiopathic pulmonary fibrosis

被引:50
作者
Bargagli, E. [1 ]
Olivieri, C. [1 ]
Nikiforakis, N. [1 ]
Cintorino, M. [2 ]
Magi, B. [3 ]
Perari, M. G. [1 ]
Vagaggini, C. [1 ]
Spina, D. [2 ]
Prasse, A. [4 ]
Rottoli, P. [1 ]
机构
[1] Univ Siena, Dept Clin Med & Immunol, Resp Dis Sect, I-53100 Siena, Italy
[2] Univ Siena, Dept Pathol, I-53100 Siena, Italy
[3] Univ Siena, Dept Biol Mol, I-53100 Siena, Italy
[4] Univ Freiburg, Dept Pneumol, Freiburg, Germany
关键词
Macrophage migration inhibitory factor; Bronchoalveolar lavage; Lung tissue; Interstitial lung diseases; Idiopathic pulmonary fibrosis; BRONCHOALVEOLAR LAVAGE; PROTEOME ANALYSIS; FACTOR GENE; PATHOGENESIS; SARCOIDOSIS; EXPRESSION; DISEASE; ANTIGEN; KINASE; SERUM;
D O I
10.1016/j.resp.2009.05.004
中图分类号
Q4 [生理学];
学科分类号
071003 [生理学];
摘要
By proteomic approach we previously characterised bronchoalveolar lavage (BAL) protein profiles of patients with idiopathic pulmonary fibrosis (IPF), sarcoidosis and systemic sclerosis. Among differently expressed proteins we identified macrophage migration inhibitory factor (MIF), a multi-function pleiotropic cytokine. This study was performed to validate our findings by a further proteomic approach and ELISA in a larger population of patients and controls. MIF expression in lung tissue was also evaluated by immunohistochemistry. MIF was identified in all 2-DE gels of IPF patients and it was significantly increased compared to controls (p < 0.05). This result was confirmed by ELISA: MIF concentrations were significantly higher in IPF patients than controls (p < 0.001) and were directly correlated with neutrophil percentages (p = 0.0095). Immunohistochemical analysis revealed enhanced expression in bronchiolar epithelium, alveolar epithelium, and fibroblastic foci. In conclusion, MIF is a pleiotropic cytokine that could be involved in the pathogenesis of IPF, being particularly abundant in BAL of these patients and mainly expressed in the areas of active fibrosis. (C) 2009 Elsevier B.V. All rights reserved.
引用
收藏
页码:261 / 267
页数:7
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