Abstract
Porphyromonas gingivalis (P.g.), which is a potential pathogen
for periodontal diseases, contains lipopolysaccharide
(LPS), and this endotoxin stimulates a variety of cellular
responses. At present, P.g.-derived LPS-induced cellular responses
in human periodontal ligament fibroblasts (PDLFs)
are not well characterized. Here, we demonstrate that P.gderived
LPS regulates inflammatory responses, apoptosis
and differentiation in PDLFs. Interleukin-6 (IL-6) and -8
(IL-8) were effectively upregulated by treatment of P.g.-derived
LPS, and we confirmed apoptosis markers including
elevated cytochrome c levels, active caspase-3 and morphological
change in the presence of P.g.-derived LPS. Moreover,
when PDLFs were cultured with differentiation media, P.g.-
derived LPS reduced the expression of differentiation marker
genes, as well as reducing alkaline phosphatase (ALP) activity
and mineralization. P.g.-derived LPS-mediated these
cellular responses were effectively abolished by treatment
of mitogen-activated protein kinase (MAPK) inhibitors.
Taken together, our results suggest that P.g.-derived LPS
regulates several cellular responses via activation of MAPK
signaling pathways in PDLFs.
Citations
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