Functional role of interleukin 1 in periodontal disease: induction of interleukin 1 production by Bacteroides gingivalis lipopolysaccharide in peritoneal macrophages from C3H/HeN and C3H/HeJ mice

  title={Functional role of interleukin 1 in periodontal disease: induction of interleukin 1 production by Bacteroides gingivalis lipopolysaccharide in peritoneal macrophages from C3H/HeN and C3H/HeJ mice},
  author={Shigemasa Hanazawa and Kohjin Nakada and Yoshihiro Ohmori and Takehito Miyoshi and Shigeru Amano and Shigeo Kitano},
  journal={Infection and Immunity},
  pages={262 - 270}
Hot phenol-water-extracted lipopolysaccharide (LPS) from Bacteroides gingivalis 381 was purified by Sephadex G-100 chromatography with Tris buffer supplemented with sodium deoxycholate and EDTA (B-LPS). In the present study, B-LPS was examined for its ability to induce interleukin 1 (IL-1) production, a mitogenic response, and macrophage activation in LPS high-responder C3H/HeN and low-responder C3H/HeJ mice. A significant increase in IL-1 production was observed in C3H/HeN and C3H/HeJ… 

Stimulation of interleukin-1 production and activation of macrophage functions by Bacteroides gingivalis

Results show that B. gingivalis has the ability to induce functional activation of mouse peritoneal macrophages, which suggests that similar activation of macrophage may occur in lesions of periodontal disease.

Bacteroides gingivalis stimulates bone resorption via interleukin-1 production by mononuclear cells. The relative role for B. gingivalis endotoxin.

The data suggest that human peripheral blood cells confronted with B. gingivalis produce large amounts of IL-1 which has strong osteoclast stimulating activity, however, in contrast with E. coli LPS, B.GingivalIS LPS does not seem to be the major inducing agent, and other bacterial components must be responsible for the observed IL- 1 and OAF induction.

Effect of lipopolysaccharide from Porphyromonas gingivalis on prostaglandin E2 and interleukin-1-beta release from rat periosteal and human gingival fibroblasts in vitro.

Results demonstrate that LPS from P. gingivalis is capable of stimulating PGE2 and IL-1 beta release from fibroblasts, which would appear to be an additional mechanism by which LPS can induce tissue breakdown in periodontal disease.

Production of Interleukin-1 and Tumor Necrosis Factor by Human Peripheral Monocytes Activated by Periodontal Bacteria and Extracted Lipopolysaccharides

Results indicate that monocytes are activated by free LPS or LPS bound to Gram-negative pathogenicperiodontal bacteria to produce monokines which may contribute to the destruction of periodontal bone.

LPS-elicited secretory responses in monocytes: altered release of PGE2 but not IL-1 beta in patients with adult periodontitis.

Findings indicate that LPS-stimulated PGE2 release from peripheral blood monocytes may correlate with susceptibility to periodontitis in human subjects.

Lipopolysaccharide (LPS)-induced cell death of C3H mouse peritoneal macrophages in the presence of cycloheximide: different susceptibilities of C3H/HeN and C3H/HeJ mice macrophages

The results suggest that this cytotoxicity might be partially regulated by high concentrations of exogenous TNF-α in both C3H/HeN and C3h/HeJ macrophages, implying a possibility of paracrine regulation of TNF -α in mice toward LPS-treated macrophage under impaired protein synthesis.

Bacteroides (Porphyromonas) gingivalis fimbriae activate mouse peritoneal macrophages and induce gene expression and production of interleukin-1

Observations suggest that B. gingivalis fimbriae may be involved in the pathogenesis of adult periodontal disease via triggering of IL-1 production by monocytes/macrophage activation of peritoneal macrophages inperiodontal diseases.

Differential Expression of IL-1β, TNF-α, IL-6, and IL-8 in Human Monocytes in Response to Lipopolysaccharides from Different Microbes

The results demonstrate that monocyte activation and cytokine release depend on the physicochemical form of LPS as well as the source of monocytes, which may be significant in the pathogenesis of periodontal infections.

Inducing effect of periodontopathic bacteria on interleukin-1 production by mouse peritoneal macrophages.

Sonicated extracts from Bacteroides gingivalis. Fusobacterium nucleatum, Actinobacillus actinomycetemcomitans, and Actinomyces viscosus were found to strongly induce IL-1 production by mouse