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Serum levels, tissue expression and cellular secretion of macrophage migration inhibitory factor in limited and diffuse systemic sclerosis


1, 2, 3, 4, 5, 6, 7, 8, 9

 

  1. Department of Medicine, Surgery and Neurosciences, University of Siena, Italy.
  2. Department of Life Sciences, University of Siena, Italy.
  3. Research Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genova, Genova, Italy.
  4. Department of Life Sciences, University of Siena, Italy.
  5. Department of Life Sciences, University of Siena, Italy.
  6. Department of Life Sciences, University of Siena, Italy.
  7. Department of Life Sciences, University of Siena, Italy.
  8. Department of Medicine, Surgery and Neurosciences, University of Siena, Italy.
  9. Department of Medicine, Surgery and Neurosciences, University of Siena, Italy. nicola.giordano@unisi.it

CER7976
2015 Vol.33, N°4 ,Suppl.91
PI 0098, PF 0105
Diagnosis

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PMID: 26005773 [PubMed]

Received: 29/09/2014
Accepted : 13/01/2015
In Press: 25/05/2015
Published: 31/08/2015

Abstract

OBJECTIVES:
To investigate serum levels, tissue/cellular expression of macrophage migration inhibitory factor (MIF) in patients with limited (lSSc) and diffuse (dSSc) systemic sclerosis.
METHODS:
10 lSSc-patients, 10 dSSc-patients and 10 controls were enrolled. MIF serum levels were assayed by ELISA. MIF and its receptors CD74/CD44 were evaluated by immunohistochemistry on skin biopsies from patients with dSSc, lSSc (affected and not-affected skin) and controls. MIF levels were assessed (ELISA) in supernatants of healthy dermal microvascular endothelial cells (MVECs) and in control (CTR), non-affected SSc (NA) and affected (SSc) fibroblasts treated for 48h with 10% control serum and 10% SSc-serum. MIF supernatant (ELISA) and mRNA (quantitative real-time PCR) levels were determined in SSc dermal fibroblasts and in control dermal fibroblasts untreated or stimulated at 6h-24h-48h with bleomycin (50mU/ml).
RESULTS:
Serum MIF was significantly higher in dSSc (18.7±4.1 ng/ml, p<0.001) and in lSSc (10.4±4.4 ng/ml, p<0.001) patients respect to controls (2.6±1.4 ng/ml). Enhanced MIF immunoreactivity was found in keratinocytes, fibroblasts, endothelium, sebaceous/sweat glands from lSSc/dSSc affected skin. Faint MIF immunoreactivity was found in control skin and not-affected skin of lSSc patients. No differences were found in CD74/CD44 receptors’ analysis among control and dSSc/lSSc affected and non-affected skin. MVECs and fibroblasts (CTR, NA and SSc) produced significantly more MIF, when stimulated with SSc serum respect to control-serum (p<0.001). Finally, MIF mRNA levels significantly increased at 6h (p<0.001) and decreased at 48h (p<0.001) in control fibroblasts treated with bleomycin compared to control untreated. Simultaneously, MIF supernatant protein levels increased after 48h (p<0.01) in bleomycin-treated fibroblasts respect to untreated ones.
CONCLUSIONS:
These results suggest that MIF could be implicated in the pathogenesis of SSc, probably acting as protective factor against the SSc stressful conditions.

Rheumatology Article