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Xylitol Inhibits Inflammatory Cytokine Expression Induced by Lipopolysaccharide from Porphyromonas gingivalis

Xylitol Inhibits Inflammatory Cytokine Expression Induced by Lipopolysaccharide from... Porphyromonas gingivalis is one of the suspected periodontopathic bacteria. The lipopolysaccharide (LPS) of P. gingivalis is a key factor in the development of periodontitis. Inflammatory cytokines play important roles in the gingival tissue destruction that is a characteristic of periodontitis. Macrophages are prominent at chronic inflammatory sites and are considered to contribute to the pathogenesis of periodontitis. Xylitol stands out and is widely believed to possess anticaries properties. However, to date, little is known about the effect of xylitol on periodontitis. The aim of the present study was to determine tumor necrosis factor alpha (TNF- ) and interleukin-1ß (IL-1ß) expression when RAW 264.7 cells were stimulated with P. gingivalis LPS (hereafter, LPS refers to P. gingivalis LPS unless stated otherwise) and the effect of xylitol on the LPS-induced TNF- and IL-1ß expression. The kinetics of TNF- and IL-1ß levels in culture supernatant after LPS treatment showed peak values at 1 h (TNF- ) and 2 to 4 h (IL-1ß), respectively. NF- B, a transcription factor, was also activated by LPS treatment. These cytokine expressions and NF- B activation were suppressed by pretreatment with pyrrolidine dithiocarbamate (an inhibitor of NF- B). Pretreatment with xylitol inhibited LPS-induced TNF- and IL-1ß gene expression and protein synthesis. LPS-induced mobilization of NF- B was also inhibited by pretreatment with xylitol in a dose-dependent manner. Xylitol also showed inhibitory effect on the growth of P. gingivalis. Taken together, these findings suggest that xylitol may have good clinical effect not only for caries but also for periodontitis by its inhibitory effect on the LPS-induced inflammatory cytokine expression. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Clinical and Vaccine Immunology American Society For Microbiology

Xylitol Inhibits Inflammatory Cytokine Expression Induced by Lipopolysaccharide from Porphyromonas gingivalis

Xylitol Inhibits Inflammatory Cytokine Expression Induced by Lipopolysaccharide from Porphyromonas gingivalis

Clinical and Vaccine Immunology , Volume 12 (11): 1285 – Nov 1, 2005

Abstract

Porphyromonas gingivalis is one of the suspected periodontopathic bacteria. The lipopolysaccharide (LPS) of P. gingivalis is a key factor in the development of periodontitis. Inflammatory cytokines play important roles in the gingival tissue destruction that is a characteristic of periodontitis. Macrophages are prominent at chronic inflammatory sites and are considered to contribute to the pathogenesis of periodontitis. Xylitol stands out and is widely believed to possess anticaries properties. However, to date, little is known about the effect of xylitol on periodontitis. The aim of the present study was to determine tumor necrosis factor alpha (TNF- ) and interleukin-1ß (IL-1ß) expression when RAW 264.7 cells were stimulated with P. gingivalis LPS (hereafter, LPS refers to P. gingivalis LPS unless stated otherwise) and the effect of xylitol on the LPS-induced TNF- and IL-1ß expression. The kinetics of TNF- and IL-1ß levels in culture supernatant after LPS treatment showed peak values at 1 h (TNF- ) and 2 to 4 h (IL-1ß), respectively. NF- B, a transcription factor, was also activated by LPS treatment. These cytokine expressions and NF- B activation were suppressed by pretreatment with pyrrolidine dithiocarbamate (an inhibitor of NF- B). Pretreatment with xylitol inhibited LPS-induced TNF- and IL-1ß gene expression and protein synthesis. LPS-induced mobilization of NF- B was also inhibited by pretreatment with xylitol in a dose-dependent manner. Xylitol also showed inhibitory effect on the growth of P. gingivalis. Taken together, these findings suggest that xylitol may have good clinical effect not only for caries but also for periodontitis by its inhibitory effect on the LPS-induced inflammatory cytokine expression.

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References (55)

Publisher
American Society For Microbiology
Copyright
Copyright © 2005 by the American Society For Microbiology.
ISSN
1556-6811
eISSN
1556-6811
DOI
10.1128/CDLI.12.11.1285-1291.2005
Publisher site
See Article on Publisher Site

Abstract

Porphyromonas gingivalis is one of the suspected periodontopathic bacteria. The lipopolysaccharide (LPS) of P. gingivalis is a key factor in the development of periodontitis. Inflammatory cytokines play important roles in the gingival tissue destruction that is a characteristic of periodontitis. Macrophages are prominent at chronic inflammatory sites and are considered to contribute to the pathogenesis of periodontitis. Xylitol stands out and is widely believed to possess anticaries properties. However, to date, little is known about the effect of xylitol on periodontitis. The aim of the present study was to determine tumor necrosis factor alpha (TNF- ) and interleukin-1ß (IL-1ß) expression when RAW 264.7 cells were stimulated with P. gingivalis LPS (hereafter, LPS refers to P. gingivalis LPS unless stated otherwise) and the effect of xylitol on the LPS-induced TNF- and IL-1ß expression. The kinetics of TNF- and IL-1ß levels in culture supernatant after LPS treatment showed peak values at 1 h (TNF- ) and 2 to 4 h (IL-1ß), respectively. NF- B, a transcription factor, was also activated by LPS treatment. These cytokine expressions and NF- B activation were suppressed by pretreatment with pyrrolidine dithiocarbamate (an inhibitor of NF- B). Pretreatment with xylitol inhibited LPS-induced TNF- and IL-1ß gene expression and protein synthesis. LPS-induced mobilization of NF- B was also inhibited by pretreatment with xylitol in a dose-dependent manner. Xylitol also showed inhibitory effect on the growth of P. gingivalis. Taken together, these findings suggest that xylitol may have good clinical effect not only for caries but also for periodontitis by its inhibitory effect on the LPS-induced inflammatory cytokine expression.

Journal

Clinical and Vaccine ImmunologyAmerican Society For Microbiology

Published: Nov 1, 2005

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