The Passage of Tritiated Bacterial Endotoxin across Intact Gingival Crevicular Epithelium

Schwartz, Joseph B.; Stinson, Frederick L.; Parker, R. B.

doi:10.1902/jop.1972.43.5.270

Cited by 191 publications

(83 citation statements)

References 13 publications

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“…However, concentrations of soluble CD14 (sCD14), LPS-binding protein, and antibodies to LPS of periodontal pathogens are elevated in periodontal patients compared with periodontally healthy subjects. 36 -38 LPS from dental plaque has also been shown to penetrate the gingiva, 39 and occurrence of bacteremia (number of species and positive cultures) increases with increasing severity of gingival inflammation. 40 Therefore, our results, for the first time to our knowledge, suggest that high serum concentrations of LPS are actually associated with the area of affected tissue in periodontitis.…”

Section: Discussionmentioning

confidence: 99%

Severe Periodontitis Enhances Macrophage Activation via Increased Serum Lipopolysaccharide

Pussinen

Vilkuna-Rautiainen

Alfthan

et al. 2004

ATVB

125

138

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Objective-In periodontitis, overgrowth of Gram-negative bacteria and access of lipopolysaccharide (LPS) to circulation may activate macrophages leading to foam cell formation. We investigated whether periodontal treatment affects proatherogenic properties of low-density lipoprotein (LDL) and, thus, macrophage activation. Methods and Results-LDL was isolated and characterized before and after treatment from 30 systemically healthy patients with periodontitis. Production of cytokines and LDL cholesteryl ester (LDL-CE) uptake by macrophages (RAW 264.7) was determined. Baseline periodontal variables correlated positively with serum LPS and C-reactive protein concentrations, as well as macrophage cytokine production and LDL-CE uptake. LPS concentration correlated positively with serum concentration of oxidized LDL and cytokine production. Higher cytokine production and LDL-CE uptake were induced by LDL isolated from patients with elevated number of affected teeth before treatment. Patients with serum LPS concentrations above the median (0.87 ng/mL) at baseline had higher serum high-density lipoprotein (HDL) cholesterol (baseline versus after treatment,

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Section: Discussionmentioning

confidence: 99%

Severe Periodontitis Enhances Macrophage Activation via Increased Serum Lipopolysaccharide

Pussinen

Vilkuna-Rautiainen

Alfthan

et al. 2004

ATVB

125

138

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“…The innate host response is critical to maintaining a clinically healthy periodontium (18,61), and studies have shown that in healthy individuals a highly orchestrated protective response is found (18,61). P. gingivalis, which resides in close proximity to the gingival epithelial cell surface, releases copious amounts of outer membrane vesicles containing LPS (23,24) which can penetrate periodontal tissue (37,39,53) and have direct inhibitory effects on the highly vascularized tissue adjacent to the tooth root surface. The interruption of endothelial cell responses to LPS is similar to earlier observations (15,35) demonstrating inhibition of IL-8 secretion after invasion of epithelial cells by viable P. gingivalis.…”

Section: Fig 4 Inhibition Of P38 Map Kinase Phosphorylation By P Gmentioning

confidence: 99%

Porphyromonas gingivalisLipopolysaccharide Is Both Agonist and Antagonist for p38 Mitogen-Activated Protein Kinase Activation

Darveau¹,

Arbabi

Garcia

et al. 2002

Infect Immun

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Lipopolysaccharide (LPS) is a key inflammatory mediator. It has been proposed to function as an important molecule that alerts the host of potential bacterial infection. Although highly conserved, LPS contains important structural differences among different bacterial species that can significantly alter host responses. For example, LPS obtained from Porphyromonas gingivalis, an etiologic agent for periodontitis, evokes a highly unusual host cell response. Human monocytes respond to this LPS by the secretion of a variety of different inflammatory mediators, while endothelial cells do not. In addition, P. gingivalis LPS inhibits endothelial cell expression of E-selectin and interleukin 8 (IL-8) induced by other bacteria. In this report the ability of P. gingivalis LPS to activate p38 mitogen-activated protein (MAP) kinase was investigated. It was found that p38 MAP kinase activation occurred in response to P. gingivalis LPS in human monocytes. In contrast, no p38 MAP kinase activation was observed in response to P. gingivalis LPS in human endothelial cells or CHO cells transfected with human Toll-like receptor 4 (TLR-4). In addition, P. gingivalis LPS was an effective inhibitor of Escherichia coli-induced p38 MAP kinase phosphorylation in both endothelial cells and CHO cells transfected with human TLR-4. These data demonstrate that P. gingivalis LPS activates the LPS-associated p38 MAP kinase in monocytes and that it can be an antagonist for E. coli LPS activation of p38 MAP kinase in endothelial and CHO cells. These data also suggest that although LPS is generally considered a bacterial component that alerts the host to infection, LPS from P. gingivalis may selectively modify the host response as a means to facilitate colonization.The innate host defense system protects mammalian hosts against microbial infection through an orchestrated response to the presence of nonself components (31, 32). Lipopolysaccharide (LPS), a component of the gram-negative bacterial cell wall, is a key structure recognized by a variety of different innate host defense proteins, allowing the host to "sense" a potential bacterial infection (8,62). LPS is evolutionarily an ideal target, since it is a conserved structure found on a wide variety of pathogenic bacteria and is sufficiently different from host components to allow a safe selective response (38). However, there are important structural differences in LPS composition between different bacterial species, such as fatty acid acyl chain composition and charge, which can significantly affect the host response (33,36,42,49,64). Different binding affinities for LPS binding protein and CD14 may only partly explain the lowered inflammatory response to some LPS species that has been observed (14), consistent with the notion that the major role of LPS binding protein and CD14 is to concentrate LPS at host cell surfaces (65). Recently it has been demonstrated that cell surface Toll-like receptor (TLR) proteins participate in the ability of the host to discriminate different LPS structural f...

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“…lipopolysaccharide (LPS)] from the periodontal pockets to the blood stream [3]. In fact, LPS applied in the gingival sulcus is transferred to blood vessels 2 h after application [4]. However, it is unclear whether an elevation in serum LPS concentration following periodontitis is detrimental to the general health.…”

Section: Introductionmentioning

confidence: 99%

Effects of improvement in periodontal inflammation by toothbrushing on serum lipopolysaccharide concentration and liver injury in rats

Tomofuji

Ekuni

Sanbe

et al. 2009

Acta Odontologica Scandinavica

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The Passage of Tritiated Bacterial Endotoxin across Intact Gingival Crevicular Epithelium

Cited by 191 publications

References 13 publications

Severe Periodontitis Enhances Macrophage Activation via Increased Serum Lipopolysaccharide

Severe Periodontitis Enhances Macrophage Activation via Increased Serum Lipopolysaccharide

Porphyromonas gingivalisLipopolysaccharide Is Both Agonist and Antagonist for p38 Mitogen-Activated Protein Kinase Activation

Effects of improvement in periodontal inflammation by toothbrushing on serum lipopolysaccharide concentration and liver injury in rats

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