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

Francesca Diomede | Zendy; Maria Zingariello | Zendy; Marcos Fernando Xisto Braga Cavalcanti | Zendy; Ilaria Merciaro | Zendy; N. de Isla | Zendy; Sergio Caputi | Zendy; Patrizia Ballerini | Zendy; Oriana Trubiani | Zendy

Open Access

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

Author(s) -

Francesca Diomede,

Maria Zingariello,

Marcos Fernando Xisto Braga Cavalcanti,

Ilaria Merciaro,

N. de Isla,

Sergio Caputi,

Patrizia Ballerini,

Oriana Trubiani

Publication year - 2017

Publication title -

european journal of histochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.754

H-Index - 42

eISSN - 2038-8306

pISSN - 1121-760X

DOI - 10.4081/ejh.2017.2791

Subject(s) - porphyromonas gingivalis , tlr4 , periodontal ligament stem cells , proinflammatory cytokine , mapk/erk pathway , toll like receptor , innate immune system , microbiology and biotechnology , stem cell , chemistry , lipopolysaccharide , receptor , immunology , immune system , signal transduction , periodontitis , inflammation , biology , medicine , biochemistry , alkaline phosphatase , enzyme

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.