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)

Several proinflammatory cytokines can induce periodontal tissue destruction and are thought to be useful indicators or diagnostic markers for periodontitis. Here, we aimed to investigate whether oncostatin M (OSM) was present in gingival crevicular fluid (GCF) and to clarify the correlation of GCF OSM and interleukin-6 (IL-6) levels with the severity of periodontitis. Sixty-two sites in 14 patients were divided into 4 groups based on probing depth (PD) and bleeding on probing (BOP). GCF was collected using paper strips from clinically health sites (PD < or = 3 mm, CAL: 1-3 mm, without BOP, n = 31), mildly diseased sites (PD < or = 3 mm, CAL: 3-5 mm, with BOP, n = 11), moderately diseased sites (PD = 4-6 mm, CAL: 5-8 mm, with BOP, n = 11), and severely diseased sites (PD > 6 mm, CAL: 8-12 mm, with BOP, n = 9). IL-6 and OSM in GCF were quantified by enzyme-linked immunosorbent assay and are expressed as concentrations (pg/ml) and total amounts (pg/site). Correlations of OSM and IL-6 levels with the severity of periodontitis in all groups were determined using Spearman rank correlation (r(s)). Our results showed that OSM and IL-6 were detected in most GCF samples. The total amounts of OSM and IL-6 were significantly positive correlated with severity of diseased sites (OSM: r(s) = 0.526, p < 0.01; IL-6: r(s) = 0.729, p < 0.01). No correlations of OSM or IL-6 concentration in GCF were found with disease severity. OSM and IL-6 levels in GCF were positively correlated to each other when expressed as either concentrations or total amounts (concentrations: r = 0.485, p < 0.01; total amounts r = 0.490, p < 0.01). In conclusion, our findings suggest that IL-6 and OSM may play a role in modulating the inflammatory cascade of chronic periodontitis.
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PMID:Measurement of gp130 cytokines oncostatin M and IL-6 in gingival crevicular fluid of patients with chronic periodontitis. 1586 89

Monocytes/macrophages are key members of the innate immune system and are present in higher numbers in active periodontal lesions than in inactive sites. The aim of this study was to characterize the response of human monocyte U937 cells, differentiated into adherent macrophages by treatment with phorbol-12-myristate 13-acetate, to stimulation by Fusobacterium nucleatum ssp. nucleatum lipopolysaccharide. Attachment of (3)H-lipopolysaccharide to macrophage-like cells was partially inhibited by anti-CD14 and anti-TLR4 polyclonal antibodies. Fusobacterial lipopolysaccharide did not cause cell apoptosis or block apoptosis induced by camptothecin. Lipopolysaccharide up-regulated the secretion of the pro-inflammatory cytokines interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha as well as the chemokine interleukin-8 by macrophage-like cells. In addition, it increased phospholipase C and D activities, which likely contributed to the high levels of prostaglandin E(2) detected in the cell culture supernatant. Lastly, the amount of matrix metalloproteinase-9 produced by macrophage-like cells was significantly increased by the lipopolysaccharide treatment. Interestingly, fusobacterial cells acquired matrix metalloproteinase-9 activity following incubation in the presence of the culture supernatant of lipopolysaccharide-stimulated macrophage-like cells. In summary, the lipopolysaccharide of F. nucleatum ssp. nucleatum has a large array of biological effects on macrophage-like cells. This monocytic responsiveness to lipopolysaccharide may be a key regulator of periodontitis.
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PMID:Response of human macrophage-like cells to stimulation by Fusobacterium nucleatum ssp. nucleatum lipopolysaccharide. 1662 77

Many cardiovascular studies have suggested that 3-hydroxy-3-methylglutaryl co-enzyme A reductase inhibitors (statins) have anti-inflammatory effects independent of cholesterol lowering. As a chronic inflammatory disease, periodontitis shares some mechanisms with atherosclerosis. Since oral epithelial cells participate importantly in periodontal inflammation, we measured simvastatin effects on interleukin-6 and interleukin-8 production by cultured human epithelial cell line (KB cells) in response to interleukin-1alpha. Simvastatin decreased production, an effect reversed by adding mevalonate or geranylgeranyl pyrophosphate, but not farnesyl pyrophosphate. Simvastatin was found to reduce NF-kappaB and AP-1 promoter activity in KB cells. Dominant-negative Rac1 severely inhibited interleukin-1alpha-induced NF-kappaB and AP-1 promoter activity. Our results may indicate an anti-inflammatory effect of simvastatin on human oral epithelial cells, apparently involving Rac1 GTPase inhibition.
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PMID:Simvastatin decreases IL-6 and IL-8 production in epithelial cells. 1672 48

Periodontal disease is an infectious disease initiated by microbial plaque, which accumulates on the tooth surface at the gingival margin and induces an inflammatory reaction. The function of the inflammatory process is to protect the host, however the process may also contribute to tissue destruction. Most individuals show gingival inflammation, but only a limited number suffer from periodontitis i.e. loss of attachment. Without treatment, periodontitis will result in tooth mobility and subsequent tooth mortality. Independent of ethnicity, 10%-15% of an adult population will develop severe periodontitis The aim of this thesis has been to analyse individuals at risk for periodontal disease. Four studies have been conducted in 2 different groups of individuals with: Recurrent periodontitis kept in a maintenance care program--studies I-III. Type 2 diabetes (T2D)--study IV. In study I, the clinicaleffect of local periodontitis treatment with an antibiotic gel was investigated. In study II, the microbiologicaleffect of periodontitis treatment with the same antibiotic gel as in study I was investigated. In study III, it was investigated whether the interleukin-l (IL-1alpha and beta) and interleukin-6 (IL-6) gene polymorphisms were associated with the susceptibility of chronic periodontitis. In study IV, the prevalence of periodontitis in individuals with T2D was investigated, together with the prevalence of diabetic complications in relation to periodontal disease. We also studied whether there was a difference in dental care habits and knowledge of oral health between T2D subjects with and without periodontal disease. In conclusion, this thesis did not find any significant clinical and microbiological differences between subjects with recurrent periodontal disease treated with a locally delivered metronidazole gel compared to a placebo gel. Neither could we find an association between genetic variants in the IL-lalpha, IL-beta and IL-6 genes in individuals with or without periodontal disease. The prevalence of severe periodontitis, according to radiographic criteria, was almost 20% in subjects with T2D. This was further confirmed by clinical parameters. T2D individuals with periodontal disease demonstrated a higher HbAlc level, a higher prevalence of cardiovascular complications and a higher proportion of smokers compared to periodontally healthy T2D subjects. Finally, T2D individuals seem to lack sufficient knowledge about oral health.
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PMID:Studies on periodontitis and analyses of individuals at risk for periodontal diseases. 1683 63

The aim of this study was to identify salivary immunoglobulin A (IgA) directed to oral microbial GroEL in patients with periodontitis and to demonstrate their potential protective role through a reduction of inflammatory cytokine production induced by microbial GroEL. Using five different proteins belonging to the heat-shock protein 60 family, Western immunoblot analysis of salivary IgA from 63 subjects revealed immunoreactivities with Campylobacter rectus GroEL and Porphyromonas gingivalis GroEL in subjects with periodontitis (P < 0.05) compared to control subjects. Using the BIACORE 1000 to measure the salivary IgA titers directed towards C. rectus GroEL, high resonance unit (RU) values were observed in the saliva samples from patients with periodontitis (P < 0.01). Furthermore, the number of teeth with deep pocket depth (>or=5 mm) showed a high correlation coefficient with the RU value (r = 0.50, P < 0.01). C. rectus GroEL possessed the ability to stimulate the production of interleukin-6 by gingival fibroblasts. Interestingly, salivary IgA antibody directed to C. rectus GroEL caused a partial inhibition of interleukin-6 production. This study showed a relationship between high levels of salivary IgA directed to GroEL and periodontal disease severity. Although additional investigations are required, salivary IgA to GroEL may have a protective role by reducing the inflammatory response induced by GroEL derived from periodontopathogenic bacteria.
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PMID:Salivary immunoglobulin A directed to oral microbial GroEL in patients with periodontitis and their potential protective role. 1692 27

Porphyromonas gingivalis is a Gram-negative anaerobic oral black-pigmented bacterium closely associated with chronic periodontitis. Lipopolysaccharide (LPS) derived from P. gingivalis is shown to be unusual because the LPS contains a greater number of lipid A species, such as tri-, tetra-, and/or penta-acylated lipid As. In this study, a lipid A possessing penta-fatty acyl chains derived from P. gingivalis strain 381 (compound PG-381-5FA) was synthesized, and examined for its immunobiological activities, compared with a tri-acylated lipid A (compound PG-381-3FA) synthesized previously. Compound PG-381-5FA, similar to compound PG-381-3FA, demonstrated weaker activity in a Limulus test as compared with Escherichia coli-type synthetic lipid A (compound 506). Compound PG-381-5FA, followed by compound PG-381-3FA, induced KC, interleukin-6, and tumour necrosis factor-alpha production in peritoneal macrophages from LPS-responsive C3H/HeN mice, but not in those from LPS-hyporesponsive C3H/HeJ mice. Furthermore, compound PG-381-5FA, as well as compound PG-381-3FA, activated nuclear factor-kappaB via Toll-like receptor (TLR)4/mD-2, but not TLR2, in a manner similar to compound 506, and worked as an antagonist for compound 506-induced cell activation. In the case of human peripheral blood mononuclear cells, compound PG-381-5FA showed much stronger IL-6-inducing activity than compound PG-381-3FA. The present results demonstrate that the chemical synthesis of a penta-acylated lipid A, mimicking the natural lipid A portion of LPS from P. gingivalis, is attributable to immune cell activation through TLR4, similar to that of compound 506.
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PMID:Toll-like receptor 4-dependent recognition of structurally different forms of chemically synthesized lipid As of Porphyromonas gingivalis. 1733 58

Growing evidence suggests that individual genetic susceptibility may influence the host's response to infections. The aim of this project was to study whether gene polymorphisms of inflammatory markers are associated with the presence of viable periodontopathogenic bacteria. We extracted genomic DNA from 45 young adults diagnosed with generalized aggressive periodontitis to study Fc receptors, formyl peptide receptor, Interleukin-6, tumor necrosis factor-alpha, and vitamin D receptor polymorphisms. The presence and viable numbers of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Tannerella forsythensis were determined by culture, and their identities confirmed by PCR. Multiple logistic regressions revealed that both Fcgamma receptor and IL-6 -174 polymorphisms were associated with increased odds of detecting A. actinomycetemcomitans, P. gingivalis, and T. forsythensis after adjustment for age, ethnicity, smoking, and periodontitis extent. These findings support the hypothesis that complex interactions between the microbiota and host genome may be at the basis of susceptibility to aggressive periodontitis.
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PMID:Gene polymorphisms and the prevalence of key periodontal pathogens. 1745 60

Metabolic syndrome and type 2 diabetes (T2DM) resulting from sustained hyperglycemia are considered as risk factors for cardiovascular disease (CVD) but the mechanism for their contribution to cardiopathogenesis is not well understood. Hyperglycemia induces nonenzymatic glycation of protein-yielding advanced glycation end products (AGE), which are postulated to stimulate interleukin-6 (IL-6) expression, triggering the liver to secrete tissue necrosis factor alpha (TNF-alpha) and C-reactive protein (CRP) that contribute to CVD pathogenesis. Although the high prevalence of periodontitis among individuals with diabetes is well known by dental researchers, it is relatively unrecognized in the medical community. The expression of the same proinflammatory mediators implicated in hyperglycemia (i.e., IL-6, TNF-alpha, and CRP) have been reported to be associated with periodontal disease and increased risk for CVD. We will review published evidence related to these 2 pathways and offer a consensus.
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PMID:Oral infection, hyperglycemia, and endothelial dysfunction. 1790 6

Periodontitis is an inflammatory process that ultimately results in tooth loss. Although the primary etiologic agent for periodontitis is bacteria, the majority of periodontal tissue destruction is thought to be caused by an inappropriate host response. Reactive oxygen species (ROS) have been known to be involved in periodontal tissue destruction. We treated human gingival fibroblasts with lipopolysaccharide (LPS) obtained from E. coli and the periodontopathogens Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis, and examined their inflammatory responses in the presence and absence of the antioxidant N-acetylcysteine (NAC). LPS enhanced ROS production, as well as, expression of pro-inflammatory cytokines such as interleukin-1beta, interleukin-6, interleukin-8 and tumor necrosis factor-alpha, and the production and activation of MMP2. NAC suppressed all LPS-induced inflammatory responses examined, suggesting that LPS-induced ROS may play a major regulatory role in these responses in gingival fibroblasts. In addition, NAC prevented LPS-induced activation of p38 MAPK and JNK but not phosphorylation and subsequent degradation of IkB. These results indicate that NAC exerts anti-inflammatory effects in LPS-stimulated gingival fibroblasts, functioning at least in part via down-regulation of JNK and p38 MAPK activation. Furthermore, this work suggests that antioxidants may be useful in adjunctive therapies that complement conventional periodontal treatments.
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PMID:N-acetylcysteine prevents LPS-induced pro-inflammatory cytokines and MMP2 production in gingival fibroblasts. 1803 7

The purpose of this study was to evaluate endothelial function in patients with periodontitis. We evaluated forearm blood flow responses to acetylcholine and sodium nitroprusside in patients with periodontitis who had no other cardiovascular risk factors (32 men; 25+/-3 years of age), in a normal control group (20 men; 26+/-3 years of age), and in hypertensive patients with periodontitis (28 men and 10 women; 56+/-12 years of age) and without periodontitis (control group; 18 men and 6 women; 54+/-13 years of age). Forearm blood flow was measured using strain-gauge plethysmography. Circulating levels of C-reactive protein and interleukin-6 were significantly higher in the periodontitis group than in the control group. Both in healthy and hypertensive subjects, forearm blood flow responses to acetylcholine were significantly smaller in the periodontitis group than in the control group. Sodium nitroprusside-stimulated vasodilation was similar in the 2 groups. Periodontal therapy reduced serum concentrations of C-reactive protein and interleukin-6 and augmented acetylcholine-induced vasodilation in periodontitis patients with and without hypertension. After administration of N(G)-monomethyl-L-arginine, an NO synthase inhibitor, forearm blood flow response to acetylcholine was similar before and after treatment. These findings suggest that periodontitis is associated with endothelial dysfunction in subjects without cardiovascular risk factors, as well as hypertensive patients, through a decrease in NO bioavailability and that systemic inflammation may be, at least in part, a cause of endothelial dysfunction, leading to cardiovascular diseases.
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PMID:Periodontal infection is associated with endothelial dysfunction in healthy subjects and hypertensive patients. 1803 79


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