Antagonistic effect of peptidoglycan of Streptococcus sanguinis on lipopolysaccharide of major periodontal pathogens

Abstract

Streptococcus sanguinis is often found in subgingival biofilm including periodontopathogens, and is correlated with a delay in colonization by periodontopathogens. However, the effect of S. sanguinis on inflammation induced by periodontopathogens is poorly understood. Thus, this study investigated the effect of S. sanguinis peptidoglycan (PGN) on induction of TNF-α, IL-6, and IL-8 expression by lipopolysaccharide (LPS) of periodontal pathogens. LPS was extracted from Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Tannerella forsythia, and PGN was isolated from S. sanguinis. THP-1 cells, a monocytic cell-line, were cotreated with LPS of the periodontal pathogens and S. sanguinis PGN, and then the expression of inflammatory cytokines was analyzed by real-time RT-PCR. To analyze the underlying mechanism, the binding assay of the LPS to CD14 or LPS-binding protein (LBP) was performed in the presence or absence of the PGN after coating recombinant human CD14 and LBP on EIA plate. The PGN inhibited the binding of LPS to CD14 and LBP in a dose-dependent manner. Also, THP-1 cells were co-treated with the LPS in the presence of N-acetylmuramic acid and N-acetylglucosamine, as components of PGN, and the competition binding assay to CD14 and LBP was performed. N-acetylmuramic acid inhibited the induction of inflammatory cytokine expression by LPS and the binding of LPS to CD14 or LBP whereas N-acetylglucosamine did not show such effect. Collectively, the results suggest that S. sanguinis PGN inhibited the cytokine expression induced by the LPS of periodontopathogens due to the inhibition of LPS binding to LBP and CD14. N-acetylmuramic acid of PGN may play a role in inhibition of the LPS binding of periodontopathogens to CD14 and LBP.

Bacterial Adhesion on Lithium Disilicate Ceramic Surface Exposed to Different Hydrofluoric Solutions

“…This bacterium is responsible for biofilm formation which causes periodontal problems and tooth decay [23]. Therefore, it is necessary to diminish factors that lead to the adhesion of these first-colonizer bacteria, thus avoiding the maturation of the biofilm which could develop into oral diseases and clinical failures of ceramic restorations.…”

“…After the immersions were performed, the lithium disilicate discs were sterilized in gamma radiation (14.5 ± 0.05 kGy) for the subsequent performance of microbiological analysis [23], which was performed in triplicate, in three independent experiments (n = 9). The Streptococcus sanguinis IAL 1832 strain was used.…”

Inhibitory effect of <i>Lactococcus lactis</i> on the bioactivity of periodontopathogens

“…LPS was extracted from F. nucleatum, P. gingivalis, T. forsythia, and T. denticola by an LPS extraction kit with little modification as described by Lee (2015). After cultivation in the respective media, the periodontopathogens were harvested by centrifugation at 6,500 ¥ g for 10 min at 4∞C and then washed with cold phosphate buffered saline (PBS; pH 7.0).…”

“…The lipopolysaccharide (LPS) of these bacteria acts as an immune stimulator by inducing gingival inflammation and activating osteoclasts via Toll-like receptors (TLR2 or TLR4) that trigger the expression of various cytokines, which in turn causes alveolar bone resorption (Kim and Lee, 2014;Lee, 2015;Lee and Baek, 2013;Socransky et al, 1998). Another characteristic of periodontopathogens is their ability to induce halitosis, an oral malodor.…”

Influence of a light‐activated glaze on the adhesion of Streptococcus sanguinis to the surface of polymers used in fabrication of interim prostheses

“…Streptococcus sanguinis is among the early colonizers of the plaque . It is a commensal microorganism often found in the subgingival biofilm, along with periodontopathogens …”