Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the production of interleukin-6 (IL-6) by human gingival fibroblasts (ATCC CRL 1292) stimulated with lipopolysaccharide (LPS) from Porphyromonas gingivalis and Escherichia coli, or supernatant of human peripheral blood adherent cell culture medium incubated in the presence of IL-1 and the same two LPS. Confluent monolayers of gingival fibroblasts were incubated with stimulants for 6 h at 37 degrees C in 5% CO2 and air. After removal of stimulants, the cell cultures were incubated for an additional 2 or 24 h in the same environment. At the end of the culture period, supernatants were collected and assayed for IL-6 activity by stimulatory IgG production with the human B-lymphoblastoid cell line CESS. The direct effect of LPS on IL-6 production by gingival fibroblasts was much weaker than the indirect one via IL-1 production by adherent cells. The stimulating effect of culture supernatants of adherent cells stimulated with LPS on IL-6 production by gingival fibroblasts was as effective as that of recombinant IL-1, when this latter was added at a concentration equivalent to that contained in the culture supernatant of adherent cells. These results suggest that, although gingival fibroblasts may be involved in the pathogenesis of chronic periodontal disease by the production of cytokines, such a role may not result from a direct stimulation by periodontopathic bacteria. The phenomenon is more likely to be mediated indirectly by IL-1 produced by infiltrating inflammatory cells.
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PMID:Direct and indirect effects of Porphyromonas gingivalis lipopolysaccharide on interleukin-6 production by human gingival fibroblasts. 132 99

This study was performed to investigate the aspects of interleukin-6 (IL-6) production in both the gingival tissue and the peripheral blood of patients with periodontal disease and of periodontally healthy subjects. In addition, IL-6 expression in human gingival tissues was studied by reverse transcription-polymerase chain reaction analysis and by immunoperoxidase staining with anti-IL-6 monoclonal antibody. The levels of IL-6 in the culture supernatants from peripheral blood mononuclear cells (PBMC) stimulated with lipopolysaccharide and in serum were examined by bioassay. We detected IL-6 mRNA expression in all inflamed gingival tissues (17/17) examined and in 2/4 in healthy gingival tissues. IL-6 protein was detected mainly in endothelial cells, fibroblasts, and macrophages but not in the area containing T or B cells in the inflamed gingival tissues, and was not detected at all in healthy gingival tissues. There was no significant difference between the subjects with periodontal disease and those with healthy gingival tissues either in serum IL-6 levels or in the amount of IL-6 produced by PBMC. These results suggest that non-lymphoid cells in inflamed gingival tissue may contribute to the pathogenesis of periodontal disease via IL-6 production, and that the IL-6 produced in gingival tissue may not reflect the IL-6 levels in peripheral blood.
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PMID:Assessment of interleukin-6 in the pathogenesis of periodontal disease. 815 11

This paper describes a study of whether or not the amounts of interleukin-6 (IL-6) in gingival crevicular fluid (GCF) are correlated with periodontal clinical measures. A sensitive ELISA was developed to measure IL-6 in GCF. Two male and 3 female adult subjects with periodontal disease were examined at their first appointments, after 3 months, and after 6 months. Data were obtained on plaque index (PI), bleeding index (BI), probing depth (PD), and on the IL-6 content of GCF samples from 16 sites per subject for a total of 240 measurements. Significant correlations were found between BI and IL-6 (P < 0.005) and between PD and IL-6 (P < 0.05), but not between PI and IL-6. Only 6 out of the 80 sites (in 3 of the 5 subjects) showed PD increases of at least 2 mm. However, for each of these 3 subjects, the amounts of IL-6 in the GCF samples from these sites were markedly higher than the mean amounts of IL-6 in the GCF samples from the remaining sites. These findings suggest that IL-6 may be a useful indicator of periodontal disease, although more extensive longitudinal studies are needed to determine the real clinical value of this GCF component.
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PMID:Measurements of interleukin-6 in gingival crevicular fluid from adults with destructive periodontal disease. 827 8

This single-blind, 8-week study compared the efficacy of a sonic toothbrush and a manual brush in 40 patients with adult periodontitis. Qualitative clinical indices and quantitative laboratory methods were used to monitor the periodontal status of 3 pockets 5 to 7 mm deep in each subject. Patients were randomly assigned either a sonic or manual toothbrush. The two groups were comparable with respect to age, gender, and anatomical location of the test sites. Data were collected from all sites at baseline and at 2, 4, and 8 weeks. Over the 8-week period, both groups showed significant improvements in the clinical indices used. Descriptive statistics indicated the sonic brush group had greater improvement than the manual group in the clinical parameters (gingival index, bleeding index, probing depth, and clinical attachment level). Gingival crevicular fluid (GCF) flow was significantly lower in the sonic brush group (P = 0.018). Considerable variation was present in the levels detected for both inflammatory cytokines tested, however, concentration of interleukin-1 beta was significantly lower in the GCF of sonic group patients (P = 0.05), while concentration of interleukin-6 was significantly reduced in both groups (P < or = 0.05) (t tests). Under these conditions, there is some evidence to suggest that the sonic toothbrush is more beneficial in resolving inflammation in patients with moderate periodontal disease.
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PMID:Efficacy of a sonic toothbrush on inflammation and probing depth in adult periodontitis. 888 48

In the present study, we examined mechanisms of Porphyromonas gingivalis lipopolysaccharide (P-LPS)-stimulated bone resorption via CD14, one of the lipopolysaccharide (LPS) receptors, and also assessed the inhibitory action of several kinds of antibiotics on the LPS-induced stimulation. First, we observed by using mouse embryonic calvarial cells that P-LPS stimulated bone resorption through the action of endogenous interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) via CD14 because (i) P-LPS-stimulated expression of IL-1beta and IL-6 genes in calvarial cells was inhibited by an anti-mouse CD14 antibody, (ii) stimulated bone resorption was markedly inhibited by both IL-1beta and IL-6 antibodies, and (iii) P-LPS-stimulated bone resorption was clearly neutralized by an anti-mouse CD14 antibody. Next, we examined the effects of several kinds of antibiotics on P-LPS-stimulated bone resorption via CD14. Two of them, chloramphenicol and erythromycin, inhibited P-LPS-stimulated bone resorption in a dose-dependent manner. In an additional experiment, we observed that chloramphenicol clearly inhibited P-LPS-stimulated expression of the CD14, IL-1beta, and IL-6 genes in calvarial cells. These results suggest that chloramphenicol might be a useful antibiotic as an anti-inflammatory agent against P-LPS-stimulated periodontal destruction occurring via CD14 in periodontal disease.
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PMID:Porphyromonas gingivalis lipopolysaccharide-stimulated bone resorption via CD14 is inhibited by broad-spectrum antibiotics. 928 14

There is little information concerning the incidence of alveolar bone loss in estrogen-deficient women. Ovariectomized sheep are valid models for study of the effects of estrogen deficiency on bone metabolism. The objective of this study was to compare alveolar bone loss in control (C) and ovariectomized sheep (OVX) at 3 and 12 months following surgery. OVX animals had decreased serum levels of 17-beta-estradiol and increased serum levels of osteocalcin, IL-6, and urinary levels of deoxypyridinoline which, taken together, suggest development of osteoporosis. The mean probing depths and percentage of sites with pocket depths 4 to 6 mm and > 6 mm were significantly greater in OVX than C at each time period and in OVX were significantly greater at 12 months that at 3 months. Gingival tissue interleukin-6 (IL-6) levels (but not the number of IL-6(+) cells) were elevated adjacent to deep periodontal pockets; however, there was no significant elevation of levels of the proinflammatory cytokines IL-1 beta and IL-8 within gingiva. Taken together, the data suggest a systemic contribution for progression of periodontal disease associated with estrogen deficiency. This may involve upregulation of systemic IL-6 synthesis and transfer to gingiva in serum, resulting in enhanced IL-6 accumulation within the gingival tissues or reduced bone density allowing for a greater amount of alveolar bone loss.
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PMID:Alveolar bone loss one year following ovariectomy in sheep. 937 31

Based upon the prosthodontic literature, subjects who are at the transition stage between natural dentition and edentulism are called "terminal dentition" (TD) cases. The aim of the present cross-sectional investigation was to characterize the local and systemic inflammatory responses in 2 groups of patients with terminal dentition periodontitis. Eight severe adult periodontitis terminal dentition (AP-TD) subjects and 8 early onset periodontitis terminal dentition (EOP-TD) subjects were entered into the study. Our purpose was to measure an extended battery of cytokines in the gingival crevicular fluid (GCF) and in lipopolysaccharide (LPS)-stimulated monocytic culture supernatants as well as gingival mononuclear cell messenger RNA (mRNA) transcripts determined from biopsy samples. Within the GCF there were 3 tiers (levels) of mediators based upon approximate 10-fold differences in concentration. The highest tier included prostaglandin E2 (PGE2), interleukin-1 beta (IL-1 beta) and interleukin-2 (IL-2), the intermediate tier included tumor necrosis factor alpha (TNF alpha) and interferon gamma (IFN-gamma) and at the lowest concentration level were interleukin-4 (IL-4) and interleukin-6 (IL-6). Thus, the GCF analysis clearly indicated that in both AP-TD and EOP-TD groups the monocytic, i.e. IL-1 beta and PGE2 and Th1, i.e. IL-2 and IFN-gamma, inflammatory mediator levels quantitatively dominated over the Th2 mediators, i.e. IL-4 and IL-6. LPS-stimulated monocytic release of IL-1 beta, PGE2 and TNF alpha was significantly elevated in both AP-TD and EOP-TD groups compared to those of a control group of 21 subjects with moderate to advanced adult periodontitis. The cytokine mRNA expression of isolated gingival mononuclear cells showed that in both the AP-TD and the EOP-TD groups Th1 and Th2 cytokines were expressed, with low levels of IL-4 and IL-12. In conclusion, our data suggest that this cross-sectional TD periodontitis model may reflect progressive periodontal disease associated with tooth loss. Furthermore, although Th1 cytokine levels in the GCF dominate over the Th2 response, monocytic activation provides the main source of proinflammatory mediators. In addition, LPS-stimulated peripheral blood monocytes demonstrate an upregulated inflammatory mediator secretion in the terminal dentition.
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PMID:Inflammatory mediators of the terminal dentition in adult and early onset periodontitis. 968 17

Actinobacillus actinomycetemcomitans(Aa), elaborating a multiplicity of virulence factor and tissue-damaging products, is considered an etiological agent in periodontal disease. Serotype b is the most frequently isolated serotype in localized juvenile periodontitis patients, suggesting a particularly high periodontopathic potential for serotype b strains. Interleukin-6(IL-6) plays an important role in the mediation of inflammatory and immune responses as well as in the osteoclastic bone resorption. However, there is little information regarding the effect of the different serotypes of Aa on IL-6 production by human gingival fibroblasts (HGF). Therefore, the purpose of this study was to compare the ability of the three serotypes (a, b, and c) of Aa sonicates to induce the production of IL-6 by HGF. In fibroblast cultures, confluent monolayers of HGF were incubated with sonic extracts of Aa-511 (serotype a), Aa-Y4 (serotype b), and Aa-652 (serotype c) at various concentrations for 48 h at 37 degrees C in 5% CO2 and air. At the end of the culture period, supernatants were collected and analysed for IL-6 content by using EIA and bioassay. In order to compare the effects of non-lipopolysaccharide (LPS) activation of Aa sonicates on IL-6 production by HGF, we added polymyxin B in cultures with Aa sonicates to bind LPS. The results were summarized as follows. (1) All three serotypes of Aa sonicates had similar dose-dependent stimulant effects on IL-6 production by HGF, and the biological activities of IL-6 correlated with their immunoreactivities. (2) The maximum releases of IL-6 by HGF were achieved at concentrations of 10 to 100 micrograms protein/mL of Aa sonicates, and the ability of Aa-Y4 to induce the release of IL-6 was higher than that of Aa-511 and Aa-652 at these concentrations. (3) Polymyxin B (50 micrograms/mL) effectively decreased the amounts of IL-6 produced by stimulation of the HGF with 10 micrograms protein/mL of Aa sonicates. However, the polymyxin B-treated Aa-Y4 sonicate showed a higher ability to induce the release of IL-6 than the other two strains. These results indicate that Aa-Y4 (serotype b) has a higher potency to induce HGF secretion of IL-6; thus contributing to a comparatively stronger efficacy to the destruction of periodontal tissue in periodontitis.
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PMID:[Interleukin-6 production by human gingival fibroblasts following stimulation with Actinobacillus actinomycetemcomitans]. 971 39

The native GroEL-like protein was purified from Campylobacter rectus, a putative periodontal pathogen, by affinity chromatography on ATP-agarose followed by high performance liquid chromatography on Superose 6. The purified 64-kDa protein (denatured form of GroEL-like protein) was immunoreactive by SDS-PAGE and Western immunoblotting with the monoclonal antibody directed against heat shock protein 60 of human origin. The native GroEL-like protein stimulated both interleukin-6 (IL-6) and IL-8 secretion by a confluent monolayer of human gingival fibroblast in their culture supernatant. During the 22-h incubation, the amounts of IL-6 and IL-8 were increased by 5.4- and 3.5-fold, respectively. These data suggested that the GroEL-like protein might be considered to be a virulence factor of C. rectus in periodontal disease.
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PMID:The GroEL-like protein from Campylobacter rectus: immunological characterization and interleukin-6 and -8 induction in human gingival fibroblast. 978 45

In this study, we used a mouse model to examine the role of the adaptive immune response in alveolar bone loss induced by oral infection with the human gram-negative anaerobic bacterium Porphyromonas gingivalis. Severe combined immunodeficient mice, which lack B and T lymphocytes, exhibited considerably less bone loss than did immunocompetent mice after oral infection, suggesting that lymphocytes contribute to this process. Bone loss after oral infection was decreased in mice deficient in major histocompatibility complex (MHC) class II-responsive CD4(+) T cells, but no change in bone loss was observed in mice deficient in MHC class I-responsive CD8(+) T cells or NK1(+) T cells. Mice lacking the cytokine gamma interferon or interleukin-6 also demonstrated decreased bone loss. These results suggest that the adaptive immune response, and in particular CD4(+) T cells and the proinflammatory cytokines that they secrete, are important effectors of bone loss consequent to P. gingivalis oral infection. The studies also reinforce the utility of the mouse oral infection model in dissecting the pathobiology of periodontal disease.
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PMID:CD4(+) T cells and the proinflammatory cytokines gamma interferon and interleukin-6 contribute to alveolar bone loss in mice. 1033 84


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