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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Oral+Microbiol
2017 ; 9
(1
): 1334503
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Porphyromonas gingivalis and its lipopolysaccharide differently modulate
epidermal growth factor-dependent signaling in human gingival epithelial cells
#MMPMID28748038
Elkaim R
; Bugueno-Valdebenito IM
; Benkirane-Jessel N
; Tenenbaum H
J Oral Microbiol
2017[]; 9
(1
): 1334503
PMID28748038
show ga
Periodontitis is an inflammatory disease induced by pathogenic bacteria such as
Porphyromonas gingivalis. Little is known about epidermal growth factor (EGF)
signals in human gingival epithelial cells (HGEC), which are major targets of P.
gingivalis, 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 P. gingivalis and its purified lipopolysaccharide (LPS-Pg) on EGF
signaling. HGEC were infected for 2 h in a dose-dependent manner with P.
gingivalis and with heat-killed P. gingivalis, and activated for 2 and 24 h by
1 µg/mL of purified LPS-Pg. 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 P.
gingivalis, but not with heat-killed P. gingivalis, led to significant reductions
in expression levels of mRNAs and proteins for SOCS-3, IRF-1, and EGFR, while
LPS-Pg over time significantly increased the expression of these mRNAs and
proteins. Tyrosine-phosphorylation of STAT-3 was significantly increased during
infection with P. gingivalis and activation by LPS-Pg but not modified during
infection with heat-killed P. gingivalis. This study highlights that P.
gingivalis and its purified LPS differentially modulated the expression of
proteins (SOCS-3, IRF-1, EGFR, and STAT-3) interfering with EGF signaling.
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