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Journal of immunology research
2014;2014 138751.

Proinflammatory effects of diesel exhaust nanoparticles on scleroderma skin cells.

A Mastrofrancesco, M Alfè, E Rosato, V Gargiulo, C Beatrice, G Di Blasio, B Zhang, D S Su, M Picardo, S Fiorito
Author Information
  1. A Mastrofrancesco: Laboratorio di Fisiopatologia Cutanea, Istituto Dermatologico S Gallicano, Via E. Chianesi 53, 00144 Roma, Italy.
  2. M Alfè: Istituto di Ricerche sulla Combustione (IRC), CNR, Piazzale V. Tecchio 80, 80125 Napoli, Italy.
  3. E Rosato: Dipartimento di Medicina Clinica, Università Sapienza, CNR, Viale dell'Università 37, 00185 Roma, Italy.
  4. V Gargiulo: Istituto di Ricerche sulla Combustione (IRC), CNR, Piazzale V. Tecchio 80, 80125 Napoli, Italy.
  5. C Beatrice: Istituto Motori (IM), Via Marconi 8, 80125 Napoli, Italy.
  6. G Di Blasio: Istituto Motori (IM), Via Marconi 8, 80125 Napoli, Italy.
  7. B Zhang: Shenyang National Laboratory for Materials Science, Institute of Metal Research, Chinese Academy of Sciences, Shenyang 110016, China.
  8. D S Su: Shenyang National Laboratory for Materials Science, Institute of Metal Research, Chinese Academy of Sciences, Shenyang 110016, China.
  9. M Picardo: Laboratorio di Fisiopatologia Cutanea, Istituto Dermatologico S Gallicano, Via E. Chianesi 53, 00144 Roma, Italy.
  10. S Fiorito: Dipartimento di Medicina Clinica, Università Sapienza, CNR, Viale dell'Università 37, 00185 Roma, Italy.
PMID: 24982919 DOI: 10.1155/2014/138751

Abstract

Autoimmune diseases are complex disorders of unknown etiology thought to result from interactions between genetic and environmental factors. We aimed to verify whether environmental pollution from diesel engine exhaust nanoparticulate (DEP) of actually operating vehicles could play a role in the development of a rare immune-mediated disease, systemic sclerosis (SSc), in which the pathogenetic role of environment has been highlighted. The effects of carbon-based nanoparticulate collected at the exhaust of newer (Euro 5) and older (Euro 4) diesel engines on SSc skin keratinocytes and fibroblasts were evaluated in vitro by assessing the mRNA expression of inflammatory cytokines (IL-1 α , IL-6, IL-8, and TNF-α) and fibroblast chemical mediators (metalloproteases 2, 3, 7, 9, and 12; collagen types I and III; VEGF). DEP was shown to stimulate cytokine gene expression at a higher extent in SSc keratinocytes versus normal cells. Moreover, the mRNA gene expression of all MMPs, collagen types, and VEGF genes was significantly higher in untreated SSc fibroblasts versus controls. Euro 5 particle exposure increased the mRNA expression of MMP-2, -7, and -9 in SSc fibroblasts in a dose dependent manner and only at the highest concentration in normal cells. We suggest that environmental DEP could trigger the development of SSc acting on genetically hyperreactive cell systems.

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MeSH Term

Case-Control Studies
Collagen Type I
Collagen Type III
Collagenases
Dose-Response Relationship, Drug
Fibroblasts
Gene Expression
Gene-Environment Interaction
Humans
Inflammation
Interleukin-1alpha
Interleukin-6
Interleukin-8
Keratinocytes
Nanoparticles
Particulate Matter
Primary Cell Culture
Scleroderma, Systemic
Skin
Soot
Tumor Necrosis Factor-alpha
Vascular Endothelial Growth Factor A
Vehicle Emissions

Chemicals

Collagen Type I
Collagen Type III
IL6 protein, human
Interleukin-1alpha
Interleukin-6
Interleukin-8
Particulate Matter
Soot
Tumor Necrosis Factor-alpha
VEGFA protein, human
Vascular Endothelial Growth Factor A
Vehicle Emissions
Collagenases
Journal Article
Article has an altmetric score of 11

Word Cloud

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