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Journal of Immunology Research
Volume 2014 (2014), Article ID 138751, 9 pages
Research Article

Proinflammatory Effects of Diesel Exhaust Nanoparticles on Scleroderma Skin Cells

1Laboratorio di Fisiopatologia Cutanea, Istituto Dermatologico S Gallicano, Via E. Chianesi 53, 00144 Roma, Italy
2Istituto di Ricerche sulla Combustione (IRC), CNR, Piazzale V. Tecchio 80, 80125 Napoli, Italy
3Dipartimento di Medicina Clinica, Università Sapienza, CNR, Viale dell'Università 37, 00185 Roma, Italy
4Istituto Motori (IM), Via Marconi 8, 80125 Napoli, Italy
5Shenyang National Laboratory for Materials Science, Institute of Metal Research, Chinese Academy of Sciences, Shenyang 110016, China

Received 20 February 2014; Accepted 9 May 2014; Published 1 June 2014

Academic Editor: Takemi Otsuki

Copyright © 2014 A. Mastrofrancesco et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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-1α, 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.