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MyD88/ERK/NFkB pathways and pro-inflammatory cytokines release in periodontal ligament stem cells stimulated by Porphyromonas gingivalis

Francesca Diomede, Maria Zingariello, Marcos F.X.B. Cavalcanti, Ilaria Merciaro, Jacopo Pizzicannella, Natalia de Isla, Sergio Caputi, Patrizia Ballerini, Oriana Trubiani
  • Maria Zingariello
    University "Campus Bio-Medico", Laboratory of Microscopy and Ultrastructural Analysis, Italy
  • Marcos F.X.B. Cavalcanti
    Nove de Julho University, Laboratory of biophotonics applied to health sciences, Brazil
  • Ilaria Merciaro
    University “G. d’Annunzio” Chieti-Pescara, Department of Medical, Oral and Biotechnological Sciences, Italy
  • Jacopo Pizzicannella
    University “G. d’Annunzio” Chieti-Pescara, Department of Medical, Oral and Biotechnological Sciences, Italy
  • Natalia de Isla
    Université de Lorraine, CNRS, UMR 7365 Ingénierie Moléculaire et Physiopathologie Articulaire (IMOPA), France
  • Sergio Caputi
    University “G. d’Annunzio” Chieti-Pescara, Department of Medical, Oral and Biotechnological Sciences, Italy
  • Patrizia Ballerini
    University “G. d’Annunzio” Chieti-Pescara, Department of Psychological, Health and Territorial Sciences, Italy

Abstract

The present study was aimed at investigating whether human Periodontal Ligament Stem Cells (hPDLSCs) were capable of sensing and reacting to lipopolysaccharide from Porphyromonas gingivalis (LPS-G) which is widely recognized as a major pathogen in the development and progression of periodontitis. At this purpose hPDLCs were stimulated with 5 μg/mL LPS-G various times and the expression of toll-like receptor 4 (TLR4) was evaluated. Toll-like receptors (TLRs) play an essential role in innate immune signaling in response to microbial infections, and in particular TLR4, type-I transmembrane proteins, has been shown recognizing LPS-G. Our results put in evidence, in treated samples, an overexpression of TLR4 indicating that, hPDLSCs express a functional TLR4 receptor. In addition, LPS-G challenge induces a significant cell growth decrease starting from 24 h until 72 h of treatment. LPS-G leads the activation of the TLR4/MyD88 complex, triggering the secretion of proinflammatory cytokines cascade as: IL-1α, IL-8, TNF-α and β and EOTAXIN. Moreover, the upregulation of pERK/ERK signaling pathways and NFkB nuclear translocation was evident. On the basis of these observations, we conclude that hPDLSCs could represent an appropriate stem cells niche modeling leading to understand and evaluate the biological mechanisms of periodontal stem cells in response to LPS-G, mimicking in vitro an inflammatory process occurring in vivo in periodontal disease.

Keywords

MyD88; ERK; NFkB; cytokines; LPS-G; hPDLSCs.

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Submitted: 2017-03-16 13:27:44
Published: 2017-05-24 08:57:42
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Copyright (c) 2017 Francesca Diomede, Maria Zingariello, Marcos F.X.B. Cavalcanti, Ilaria Merciaro, Jacopo Pizzicannella, Natalia de Isla, Sergio Caputi, Patrizia Ballerini, Oriana Trubiani

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