Effects of Butyrate and Propionate on the Adhesion, Growth, Cell Cycle Kinetics, and Protein Synthesis of Cultured Human Gingival Fibroblasts

Jeng, Jiiang‐Huei; Chan, Chiu Po; Ho, Yuan Soon; Lan, Wan–Hong; Hsieh, C.C.; Chang, Mei Chi

doi:10.1902/jop.1999.70.12.1435

Cited by 52 publications

(55 citation statements)

References 27 publications

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“…The PI fluorescence of twenty thousand cells was analyzed for both control and experimental samples. We counted the percentage of cells residing in sub-G0/G1, G0/G1 phase, S phase and G2/M phase by using ModiFit software and CellQuest programs [9,21,23].…”

Section: Cytotoxicity Of Bisgma On Dental Pulp Cellsmentioning

confidence: 99%

The role of reactive oxygen species and hemeoxygenase-1 expression in the cytotoxicity, cell cycle alteration and apoptosis of dental pulp cells induced by BisGMA

et al. 2010

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Section: Cytotoxicity Of Bisgma On Dental Pulp Cellsmentioning

confidence: 99%

The role of reactive oxygen species and hemeoxygenase-1 expression in the cytotoxicity, cell cycle alteration and apoptosis of dental pulp cells induced by BisGMA

et al. 2010

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“…Most subgingival species are proteolytic and produce an array of volatile fatty acids including butyrate, propionate, and isobutyrate (85,208,261), as well as sulfides such as hydrogen sulfide and methyl mercaptan, as metabolic by-products (226,227). All these compounds could be cytotoxic to the gingival tissue, based on tissue culture studies in which propionate and butyrate inhibited the growth of cultured epithelial and endothelial cells and fibroblasts (114,123) and in which sulfides inhibited epithelial cells (233,244).…”

Section: Nonspecific Plaque Hypothesismentioning

confidence: 99%

Periodontal Disease as a Specific, albeit Chronic, Infection: Diagnosis and Treatment

Loesche

Grossman²

2001

Clin Microbiol Rev

407

338

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Periodontal disease is perhaps the most common chronic infection in adults. Evidence has been accumulating for the past 30 years which indicates that almost all forms of periodontal disease are chronic but specific bacterial infections due to the overgrowth in the dental plaque of a finite number of mostly anaerobic species such as Porphyromonas gingivalis, Bacteroides forsythus, and Treponema denticola. The success of traditional debridement procedures and/or antimicrobial agents in improving periodontal health can be associated with the reduction in levels of these anaerobes in the dental plaque. These findings suggest that patients and clinicians have a choice in the treatment of this overgrowth, either a debridement and surgery approach or a debridement and antimicrobial treatment approach. However, the antimicrobial approach, while supported by a wealth of scientific evidence, goes contrary to centuries of dental teaching that states that periodontal disease results from a “dirty mouth.” If periodontal disease is demonstrated to be a risk factor for cardiovascular disease and stroke, it will be a modifiable risk factor since periodontal disease can be prevented and treated. Since the antimicrobial approach may be as effective as a surgical approach in the restoration and maintenance of a periodontally healthy dentition, this would give a cardiac or stroke patient and his or her physician a choice in the implementation of treatment seeking to improve the patient's periodontal condition so as to reduce and/or delay future cardiovascular events

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“…F. nucleatum can also invade host tissues and obstruct healing of damaged oral tissues (Bartold et al , 1991; Jeng et al , 1999). Infection of murine macrophages with F. nucleatum has been shown to result in NLPR3 inflammasome activation and IL-1β secretion (Taxman et al , 2012); however, the mechanism was not characterized, and infection of the preferred host cells of the bacteria, GECs, has not been previously examined.…”

Section: Introductionmentioning

confidence: 99%

Fusobacterium nucleatuminfection of gingival epithelial cells leads to NLRP3 inflammasome-dependent secretion of IL-1β and the danger signals ASC and HMGB1

Bui

Johnson

Roberts

et al. 2016

Cellular Microbiology

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Summary Fusobacterium nucleatum is an invasive anaerobic bacterium that is associated with periodontal disease. Previous studies have focused on virulence factors produced by F. nucleatum, but early recognition of the pathogen by the immune system remains poorly understood. Although an inflammasome in gingival epithelial cells (GECs) can be stimulated by danger-associated molecular patterns (DAMPs) (also known as danger signals) such as ATP, inflammasome activation by this periodontal pathogen has yet to be described in these cells. This study therefore examines the effects of F. nucleatum infection on pro-inflammatory cytokine expression and inflammasome activation in GECs. Our results indicate that infection induces translocation of NF-κB into the nucleus, resulting in cytokine gene expression. In addition, infection activates the NLRP3 inflammasome, which in turn activates caspase-1 and stimulates secretion of mature IL-1β. Unlike other pathogens studied until now, F. nucleatum activates the inflammasome in GECs in the absence of exogenous DAMPs such as ATP. Finally, infection promotes release of other DAMPs that mediate inflammation, such as high-mobility group box 1 protein and apoptosis-associated speck-like protein, with a similar time-course as caspase-1 activation. Thus, F. nucleatum expresses the pathogen-associated molecular patterns necessary to activate NF-κB and also provides an endogenous DAMP to stimulate the inflammasome and further amplify inflammation through secretion of secondary DAMPs.

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Effects of Butyrate and Propionate on the Adhesion, Growth, Cell Cycle Kinetics, and Protein Synthesis of Cultured Human Gingival Fibroblasts

Abstract: These results suggested that SCFA released by pathogenic microorganisms can contribute to the gingival tissue dysfunction and breakdown through their actions on specific biological functions of GF.

Cited by 52 publications

References 27 publications

The role of reactive oxygen species and hemeoxygenase-1 expression in the cytotoxicity, cell cycle alteration and apoptosis of dental pulp cells induced by BisGMA

The role of reactive oxygen species and hemeoxygenase-1 expression in the cytotoxicity, cell cycle alteration and apoptosis of dental pulp cells induced by BisGMA

Periodontal Disease as a Specific, albeit Chronic, Infection: Diagnosis and Treatment

Fusobacterium nucleatuminfection of gingival epithelial cells leads to NLRP3 inflammasome-dependent secretion of IL-1β and the danger signals ASC and HMGB1

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