and its lipopolysaccharide differently modulate epidermal growth factor-dependent signaling in human gingival epithelial cells.
Fiche publication
Date publication
janvier 2017
Journal
Journal of oral microbiology
Auteurs
Membres identifiés du Cancéropôle Est :
Dr BENKIRANE-JESSEL Nadia
Tous les auteurs :
Elkaim R, Bugueno-Valdebenito IM, Benkirane-Jessel N, Tenenbaum H
Lien Pubmed
Résumé
Periodontitis is an inflammatory disease induced by pathogenic bacteria such as . Little is known about epidermal growth factor (EGF) signals in human gingival epithelial cells (HGEC), which are major targets of , and how the expression of proteins participating in EGF signaling-that is, EGF-receptor (EGFR), suppressor of cytokine signaling-3 (SOCS-3), interferon regulatory factor-1 (IRF-1), and signal transducers and activators of transcription (STAT-3)-are modified. This study aimed to assess the effects of and its purified lipopolysaccharide (LPS-) on EGF signaling. HGEC were infected for 2 h in a dose-dependent manner with and with heat-killed , and activated for 2 and 24 h by 1 µg/mL of purified LPS-. Quantitative reverse transcription polymerase chain reaction and Western blotting were performed to measure mRNA and protein levels for SOCS-3, IRF-1 EGF, EGFR, and STAT-3. The tyrosine-phosphorylation status of STAT-3 was also examined. The results showed that infection of HGEC cells with , but not with heat-killed , led to significant reductions in expression levels of mRNAs and proteins for SOCS-3, IRF-1, and EGFR, while LPS- over time significantly increased the expression of these mRNAs and proteins. Tyrosine-phosphorylation of STAT-3 was significantly increased during infection with and activation by LPS- but not modified during infection with heat-killed . This study highlights that and its purified LPS differentially modulated the expression of proteins (SOCS-3, IRF-1, EGFR, and STAT-3) interfering with EGF signaling.
Référence
J Oral Microbiol. 2017 ;9(1):1334503