Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relative avidity and titer of antibodies representing the 4 immunoglobulin G (IgG) subclasses (IgG1-4) reactive with Porphyromonas gingivalis, P. gingivalis-lipopolysaccharide (-LPS), streptokinase (SK) and tetanus toxoid (TT) in the sera of patients having adult periodontitis and of healthy controls were measured. Patient antibody titers to P. gingivalis and P. gingivalis-LPS were found to be significantly elevated for IgG, IgG1 (no P. gingivalis-LPS antibodies) and IgG2. The predominant antibody response to P. gingivalis and P. gingivalis-LPS occurred in the IgG2 subclass. When the relative avidity of the antibodies to P. gingivalis and P. gingivalis-LPS were examined, no significant differences between control and patient sera could be identified. However, anti-P. gingivalis and P. gingivalis-LPS antibodies were found to possess significantly lower relative avidity than either SK or TT antibodies. The IgG1 subclass antibodies to P. gingivalis, SK and TT all appeared to be of high relative avidity. In contrast, anti-P. gingivalis and P. gingivalis-LPS of the IgG2 subclass were of significantly lower relative avidity. Since the predominant humoral response to P. gingivalis occurs in the IgG2 subclass, the low relative avidity of these antibodies predominates in measurements of whole serum activity.
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PMID:Avidity and titer of immunoglobulin G subclasses to Porphyromonas gingivalis in adult periodontitis patients. 133

The extracellular release of IL-1 beta by cultured peripheral blood monocytes from 26 periodontitis patients and 26 control subjects was measured by radioimmunoassay. Unstimulated monocytes from periodontitis patients released significantly more IL-1 beta than controls during 24 h of culture; there was a wide variation in the amount of IL-1 beta released (0.45-13.00 ng/ml per 10(6) cells) which did not correlate with either the degree of bone loss or pocket formation observed clinically. When stimulated with lipopolysaccharide (LPS; Actinobacillus actinomycetemcomitans; 5 micrograms/ml) monocytes from periodontitis patients produced significantly more IL-1 beta than those from control subjects. Monocyte culture supernatants from another 10 periodontitis patients and 10 control subjects were also assayed for both IL-1 beta and TNF-alpha by enzyme-linked immunosorbent assays. Spontaneous and LPS-stimulated (Bacteroides gingivalis; 5 micrograms/ml) IL-1 beta release were again significantly higher for periodontitis patients. TNF-alpha was detected in the periodontitis cultures (0-765 pg/ml per 10(6) cells), but the mean value was not significantly different from controls. LPS-stimulated TNF-alpha release, however, was significantly higher than for control subjects, and there was a strong correlation between spontaneous IL-1 beta and TNF-alpha release by monocytes from the periodontitis group. Measurement of interferon-gamma (IFN-gamma) in lymphocyte cultures from these patients by immunoradiometric assay showed that IFN-gamma levels in periodontitis cultures were consistently low, but not significantly so when compared to controls; both groups responded equally to concanavalin-A (5 micrograms/ml). Although the precise roles of IL-1 beta and TNF-alpha in periodontitis remain unclear, these data provide evidence that both cytokines may participate in the pathogenesis of the disease.
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PMID:The release of interleukin-1 beta, tumor necrosis factor-alpha and interferon-gamma by cultured peripheral blood mononuclear cells from patients with periodontitis. 214 29

The aim of this study was to estimate the concentration of cementum-bound LPS on a group of 12 teeth that had been extracted because of periodontitis. LPS on scaled root surfaces was labelled by immunogold/silver staining. The concentrations of LPS were estimated by quantifying the amount of bound silver label, using X-ray microanalysis in areas free of plaque or calculus. These were compared against standards of known LPS concentration, which were separately prepared for each sample. Cementum-bound LPS was detected at concentrations of up to 2 EU/mm2 of affected root surface. However, most of the root surfaces had considerably lower concentrations than this, the mean of all samples never exceeding 0.7 EU/mm2. LPS concentrations were highest on cementum towards the apical regions of the affected pocket. These findings confirm that cementum-bound LPS is only present in low concentrations on affected teeth, and suggest that the clinical significance of cementum-associated LPS may have been over-estimated in the past. The demonstration of LPS appears to be more important as an indicator of retained bacteria and calculus than of cementum-bound LPS per se.
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PMID:The distribution and quantitation of cementum-bound lipopolysaccharide on periodontally diseased root surfaces of human teeth. 237 84

Serum antibody titers to lipopolysaccharide from Bacteroides intermedius (B. intermedius) and Bacteroides gingivalis (B. gingivalis) were measured by enzyme-linked immunosorbent assay in serum samples from subjects with healthy gingiva and patients with periodontitis. The IgG antibody titers to LPS from B. gingivalis were significantly higher in the patients group, compared with healthy controls. No such difference was found between IgG activity to LPS from B. intermedius in the healthy and the periodonitis. Likewise, no significant difference in specific IgA level was found between the group with healthy gingiva and the patients group, both in LPS from B. intermedius and B. gingivalis. The IgM antibody levels to LPS from B. intermedius and B. gingivalis were low in subjects of patients and controls.
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PMID:[IgG, IgA and IgM serum antibodies against lipopolysaccharide from Bacteroides intermedius in periodontal health and disease]. 248 7

Lipopolysaccharide responsiveness in human subjects was assessed through the examination of LPS-stimulated PGE2 and IL-1 beta release from counterflow isolated monocytes from patients with varying levels of periodontal destruction. This study was performed in order to investigate a possible relationship between LPS-mediated secretory responses in monocytes and susceptibility to periodontal destruction in humans. Subjects were chosen based on apparent resistance or susceptibility to disease as measured by little or no periodontal destruction versus generalized severe destruction, respectively. Because IFN-gamma can influence LPS-stimulated responses, the effect of IFN-gamma on the LPS-stimulated release of PGE2 and IL-1 beta was also assessed. Peripheral blood monocytes were separated by counterflow centrifugation and cultured (10(6)/ml/well) with control medium or medium containing LPS from Bacteroides gingivalis, B. intermedius, Actinobacillus actinomycetemcomitans, or Salmonella typhimurium, with or without 10 Units/ml recombinant IFN-gamma. Media were exchanged at 24 and 48 hours and culture supernatants assayed for both PGE2 and IL-1 beta by RIA. Patients classified as Susceptible to periodontitis demonstrated 2- to 3-fold greater PGE2 release than Resistant patients. This difference was observed with all LPS preparations over both the 0-24 hour and 24-48 h culture periods. IL-1 beta release, however, was not significantly different between patient groups. IFN-gamma did not affect the LPS-stimulated release of PGE2 but significantly enhanced the release of IL-1 beta. The IFN-gamma effects were similar for both patient groups. These findings indicate that LPS-stimulated PGE2 release from peripheral blood monocytes may correlate with susceptibility to periodontitis in human subjects.
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PMID:LPS-elicited secretory responses in monocytes: altered release of PGE2 but not IL-1 beta in patients with adult periodontitis. 252 82

The evidence that periodontitis-associated bacteria contain potent PBA factors is very strong. Clearly, antibodies directed against non-oral antigens are produced in the inflamed periodontal lesion, and PBA appears to contribute to that production. It is also clear that B cells and plasma cells are the major cell types in the periodontal lesion. Furthermore, alterations in the regulation of B-cell responses to PBA factors are associated with severe periodontal disease. However, evidence demonstrating that activated B cells and plasma cells are directly involved in the pathogenic mechanisms leading to destruction of the periodontal support is still circumstantial. Polyclonal B-cell activation and potential pathways by which PBA-stimulated cells could be involved in periodontal destruction remain largely hypothetical. It appears that IL-1 is an important osteoclast-activating agent, and that LPS, which is a potent PBA factor in many systems, can elicit IL-1 production by B cells as well as by the monocyte/macrophage lineage. Recent data indicating that IL-1 is produced by numerous malignant B-cell lines lend support for the idea that B-cell IL-1 could be important in bone resorption. It is also likely that polyclonal activation may lead to production of autoantibody such as anti-type I and anti-type III collagens, and the destruction of self tissues through ADCC reactions, immune complex formation, and complement activation. Further research is needed to determine how the B cell/plasma cell may participate in tissue injury in periodontitis, and how the B-cell response to PBA factors is regulated.
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PMID:Polyclonal B-cell activation in periodontitis. 252 22

IgG antibody levels to lipoteichoic acid (LTA), prepared from Streptococcus mutans cells, were determined by enzyme-linked immunosorbent assay in serum samples from 149 subjects. An extract from Bacteroides gingivalis and lipopolysaccharide from Escherichia coli 055:B5 served as control antigens. The reference group comprised 28 systemically and periodontally healthy adults. The main test groups were: 52 persons with gingivitis only, and 69 patients with periodontitis. Within those groups, 37 patients had insulin-dependent diabetes mellitus, another 20 patients were prospective or renal transplant recipients. The periodontitis patient group showed significantly (p less than 0.05) higher mean antibody value and higher frequency of extreme antibody responses to both LTA and B. gingivalis than the gingivitis group. LPS did not discriminate between the groups. Multiple regression analysis with gingivitis scores as the dependent variable selected plaque scores, anti-LTA antibody values and general health status as significant (p less than 0.05) regressors. The variance in radiographical alveolar bone loss was significantly (p less than 0.05) explained by age and by antibody values to B. gingivalis and to LTA. The patients with extreme immunological responsiveness to LTA or to B. gingivalis had about twice as much alveolar bone loss as those with normal serological reactivity. The results support the contention that LTA modulates the progression of periodontitis in humans.
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PMID:Serum IgG antibodies reactive with lipoteichoic acid in adult patients with periodontitis. 277 86

The biological activities of lipopolysaccharide from Bacteroides gingivalis 381 (B-LPS) were examined in vivo and in vitro. Intra-oral mucosal injection of B-LPS induced an acute inflammation at the injection site. Intravenous injection of B-LPS induced necrotic lesions with many thrombi in the liver and lymphocytic reduction in the spleen. By immunohistochemical examination, B-LPS was detected in macrophages in the liver, spleen and lymph nodes. In vitro analysis showed that B-LPS was a potent activator of both neutrophils and macrophages in luminol-dependent response and IL-1 secretion from macrophages and was mitogenic to the spleen cells not only from BALB/c mice but also from LPS-non-responder C3H/HeJ mice. Interferon production from human peripheral mononuclear leucocytes was induced, in vitro, by stimulation with B-LPS but not with the other enterobacterial LPS. These findings clarified the various biological activities of B-LPS affecting various cells and tissues, especially neutrophils, macrophages and lymphocytes. The potent inflammability of B-LPS shown in the present study indicates that it is one of the effective agents to induce periodontitis.
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PMID:Histological changes and some in vitro biological activities induced by lipopolysaccharide from Bacteroides gingivalis. 314 May 33

Endothelial cell activation by endotoxin (LPS), tumor necrosis factor (TNF), Interleukin-1-alpha, beta (IL-1-alpha, beta) and phorbolesters (TPA) results in increased monocyte adhesion. Examination of kinetics of monocyte adhesion shows that the onset of adherence enhancement (AE) is similar in all five agents (about 300% AE at 6 h), while its decrease is delayed in LPS/TNF versus IL-1-alpha, beta/TPA-induced activation (LPS versus IL-1-beta:260% versus 60% at 18 h). Monoclonal antibody (4D10), raised against 24 h LPS-stimulated endothelial cells detects an endothelial cell-specific activation antigen at Mr 81,000 that is induced by LPS, TNF, IL-1-alpha, beta and TPA (within 6 h about 100% positive cells). Decrease in antigen-positive cells is delayed in LPS/TNF versus IL-1-alpha, beta/TPA-induced antigen expression (LPS vs. IL-1-beta: 60% vs. 5% at 24 h). In situ the antigen is not expressed in normal and chronic inflammatory tissues. Acute inflammatory tissues, including contact and atopic dermatitis, psoriasis and periodontitis, however, show endothelial cells staining strongly positive. In contact eczemas at different times after elicitation (0, 6, 24, 72, 96 h), expression of the antigen is first seen after 24 h and is still strong at 96 h. These data indicate that LPS/TNF conduct an endothelial cell activation program in vitro, showing the same prolonged kinetics that is found for endothelial cell activation in the acute inflammatory process in vivo.
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PMID:Characterization and expression kinetics of an endothelial cell activation antigen present in vivo only in acute inflammatory tissues. 331 46

Using two-dimensional (2D) electrophoresis and western blot assay, we analyzed antigenic proteins in Porphyromonas gingivalis uniquely recognized by antibodies in sera of periodontitis subjects. Proteins in the total membrane fraction of P. gingivalis 381 were resolved into at least 70 protein spots by 2D electrophoresis. In the gel stained with silver, the substance around 47 kDa protein on the acidic side (at an isoelectric point of about 4.5) was stained as a smear. Antigenic substances were characterized using purified IgGs from sera of 16 adult periodontitis (AP), 19 rapidly progressive periodontitis (RPP) and 14 periodontally healthy volunteers. Western blots demonstrated that 75 kDa protein reacted with IgGs from 75% of AP patients (p < 0.001), the antigenic substance around acidic 47 kDa protein reacted with IgGs from 81.3% of AP (p < 0.01) and 68.4% of RPP patients (p < 0.01) and the acidic 47 kDa protein reacted with 87.5% of AP (p < 0.01) and 78.9% of RPP patients (p < 0.01). The reaction frequency was significantly different from that of the healthy volunteers. Also 51 kDa and 41 kDa proteins reacted with 47 and 43 of 49 IgG samples, respectively. The substance around acidic 47 kDa protein reacted with mouse antiserum to P. gingivalis-LPS. After treatment with pronase or heat, the antigenic reactions disappeared not only from the proteins, but also from the area around the acidic 47 kDa protein. When the fraction was digested with lipase, the antigenic reaction of the area decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Detection of antigenic proteins in Porphyromonas gingivalis using two-dimensional electrophoresis and western blots. 747 99


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