UMLS:C0031099 - FACTA Search

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Query: UMLS:C0031099 (periodontitis)
12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elevated numbers of plasma cells are associated with localized and chronically inflamed gingiva of patients with adult periodontitis. However, only limited information is currently available as to how cytokines produced by CD4(+) T cells are involved in these increased B cell responses in affected gingival tissues. When gingival mononuclear cells (GMC) were isolated from inflamed tissues and examined by flow cytometry, approximately 20-30% of lymphocytes were CD4(+) T cells. For the analysis of Th1 and Th2 cytokine expression by these CD4(+) T cells, RNA was extracted and reverse transcriptase-polymerase chain reaction (RT-PCR) was performed by using specific 5' and 3' primers for interferon-gamma (IFN-gamma) and IL-2 (Th1), IL-4, IL-5, IL-6, IL-10 and IL-13 (Th2) and beta-actin (internal control). Two distinct cytokine profiles were noted based on the expression of selected Th1 and Th2 cytokines, where one pattern was represented by expression of mRNA for IFN-gamma, IL-6, IL-10 and IL-13, while the second consisted of mRNA for IFN-gamma, IL-6 and IL-13. In most samples, mRNA for IL-2, IL-4 and IL-5 were not detected by cytokine-specific RT-PCR. When RNA was isolated from CD4(+) T cells of concanavalin A-stimulated peripheral blood mononuclear cells (PBMC) of the same patients and examined by RT-PCR, mRNA for all Th1 and Th2 cytokines were detected. These findings suggest that although human CD4(+) T cells are capable of producing an array of Th1- and Th2-type cytokines, the CD4(+) T cells associated with periodontitis are limited to production of IFN-gamma, IL-6, IL-13 and is some instances IL-10. CD4(+) T cells from diseased periodontal tissues are divisible into two groups based upon whether or not IL-10 is produced, together with IFN-gamma, IL-6 and IL-13.
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PMID:Selected Th1 and Th2 cytokine mRNA expression by CD4(+) T cells isolated from inflamed human gingival tissues. 860 41

An accumulation of elevated numbers of macrophages (M phi) and Ig producing cells is associated with localized and chronically inflamed gingiva of patients with adult periodontitis. When gingival lymphocytes were isolated from inflamed tissues and examined by flow cytometry, approximately 20-30% of lymphocytes were CD4+ T cells. For the analysis of Th1 and Th2 cytokine expression by these CD4+ T cells, RNA was extracted and reverse transcriptase polymerase chain reaction (RT-PCR) was performed by using specific 5' and 3' primers for IFN-gamma and IL-2 (Th1), IL-4, IL-5, IL-6, IL-10 and IL-13, (Th2) and beta-actin (housekeeping gene). Two distinct cytokine profiles were noted based on the expression of selected Th1 and Th2 cytokines. Thus, one pattern was represented by the expression of mRNA for IFN-gamma, IL-6, IL-10 and IL-13, while the other case consisted of mRNA for IFN-gamma, IL-6, and IL-13. Except for a few cases, messages for IL-2, IL-4 and IL-5 were not detected by cytokine-specific RT-PCR. The predominant expression of Th2 cytokines (e.g. IL-6, IL-10 and IL-13) may contribute to the induction of high B cell responses in local disease sites. On the other hand, lack of IL-4 may be responsible for the accumulation of M phi in diseased periodontium. We also investigated whether a relationship exists between IL-4 receptor (IL-4R) expression and M phi persistence in the absence of exogenous IL-4. Gingival M phi, when compared with monocytes (MN)/M phi from peripheral blood mononuclear cells (PBMC), expressed high levels of IL-4R mRNA. When gingival M phi were incubated with recombinant IL-4 (rIL-4), the cell viability was dramatically reduced by apoptosis. These findings clearly show that the lack of IL-4 may contribute to the persistent occurrence of M phi at the disease site and addition of exogenous rIL-4 to gingival M phi cultures leads to cell death by apoptosis.
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PMID:Molecular and cellular mechanisms for periodontal diseases: role of Th1 and Th2 type cytokines in induction of mucosal inflammation. 908 20

Previous studies have shown that type I diabetes (IDDM) increases the risk of developing periodontitis by 2-3-fold. IDDM patients exhibit destruction of the pancreatic beta cells, most probably caused by an autoimmune reaction. Evidence is accumulating to support the role of the autoimmune response in periodontal pathogenesis. A cytokine, interleukin (IL)-10, has been reported to selectively promote the expansion of a B lymphocyte lineage (CD5/LY1/B1) which has the propensity for secreting high levels of autoantibody. Therefore, the purpose of this project was to evaluate IL-10 production, percentage of CD5 B cells and the frequency of anti-collagen secreting cells in peripheral blood mononuclear cells of age, gender and race matched IDDM patients and controls. IL-10 production was evaluated by an ELISA using the supernatant of adherent peripheral blood cells cultured for 24 h in the presence of Porphyromonas gingivalis lipopolysaccharide (LPS). In 8 of 31 patients, IL-10 levels were significantly increased in IDDM compared to controls and a higher percentage of CD5 B cells was also observed by flow cytometry. In addition, these patients exhibited a higher frequency of anti-collagen secreting cells as elucidated by an ELISPOT. Moreover, treatment with a neutralizing anti-IL-10 antibody diminished the anti-collagen antibody response by 70%. These findings support the concept that a subset of IDDM patients possess an extremely robust IL-10 response following exposure to Gram-negative LPS, which could predispose them to the development of periodontitis through a heightened autoimmune mechanism.
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PMID:Interleukin-10 promotes anti-collagen antibody production in type I diabetic peripheral B lymphocytes. 908 33

In recent years advances in clinical techniques and procedures such as guided tissue regeneration and implants, have dominated periodontics. However, as we move towards the 21st century, emphasis is swinging 'back to basics' with the recognition that patient susceptibility to periodontal disease determines the ultimate outcome not only of the disease process but also of the treatment undertaken. In this context attention is returning to the host response and with the advent of clonal and molecular biological techniques, new insights are being gained into the nature of host susceptibility. Previous studies have suggested that a T-cell/macrophage immunoregulatory imbalance may exist locally in the periodontitis lesion and that this imbalance may be antigen specific. More recently, T-cell subsets have been dichotomized on the basis of their cytokine profiles. In general, Th1 cells produce IL-2 and IFN-gamma while Th2 cells produce IL-4, IL-5 and IL-6. The major function of Th1 cells is to mediate delayed type hypersensitivity. In contrast the major function of Th2 cells is to provide B-cell help. A model for periodontal disease has now been developed based on this functional dichotomy which provides a framework for the study of cytokine profiles in periodontal disease. Early studies in this context have demonstrated higher proportions of IL-4 and IL-13 producing cells in periodontitis tissues together with possible variations in IL-10 production. Clonal studies have shown that the selection of a particular cytokine profile is not antigen dependent and that differences may be due to the host susceptibility although this remains to be determined.
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PMID:Periodontics into the 21st century. 917 77

FACS analysis was used to determine the percent interferon (IFN)-gamma-, interleukin (IL)-4-, IL-10-, and CD30-positive T-cells extracted from adult periodontitis (AP) and healthy/gingivitis (H/G) subjects. Additionally, the percentages of IL-1 beta-, IL-10- and IL-12-producing B-cells and macrophages were ascertained. The percent IL-10+ CD8 cells extracted from AP lesions was decreased compared with H/G tissues (p = 0.033), and the percent CD30+ CD4 (p = 0.001) and CD30+ CD8 (p = 0.028) cells was higher in AP than in H/G tissues. The percentages of IL-1 beta + macrophages (p = 0.003) and IL-12+ B-cells (p = 0.034) were both higher in AP lesions than in H/G tissues. The specific effect of Porphyromonas gingivalis on the cytokine profiles of peripheral blood mononuclear cells isolated from P. gingivalis-infected AP and H/G patients was also determined. While there were no significant differences in the percent cytokine-positive T-cells after stimulation with P. gingivalis outer membrane antigens (OM) for 6 days compared with cells incubated in medium only, the percent CD30+ CD4 cells increased significantly (p = 0.047 and p = 0.063 for AP and H/G groups, respectively). There was also an increase in the percent IL-1 beta + B-cells from AP patients (p = 0.029), and the percent IL-12+ monocytes from AP and H/G subjects was higher than the percent IL-12+ B-cells, both after stimulation with P. gingivalis OM (p = 0.005 for the AP group and p = 0.058 and therefore not quite significant for the H/G group) and when incubated in medium alone (p = 0.016 and p = 0.015 for AP and H/G groups, respectively). This study has shown that IL-10+ CD8 cells may be significant in gingival lesions, and that CD30+ T-cells indicative of Th2 or Th0 cells may play a role in progressive periodontal disease. This study has also shown that B-cells produce IL-1 in the gingival lesion and that P. gingivalis may be significant in the induction of B-cell-induced IL-1.
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PMID:Cytokine profiles of cells extracted from humans with periodontal diseases. 943 96

It has previously been reported that, in periodontitis lesions, T cells with a memory/activated phenotype and with a type 2 cytokine profile accumulate in an oligoclonal fashion. Delineation of the role of cytokines in periodontal inflammation has, however, been complicated because of cross-regulation and because of their overlapping and often redundant effects. The aim of this study was to examine messenger RNA levels for interferon gamma, interleukin 4 (IL-4), IL-10, IL-12 and IL-13 in gingival tissues and peripheral blood mononuclear cells of patients with adult periodontitis. Reverse transcription polymerase chain reaction and subsequent image analysis was used to determine the level of mRNA for each cytokine. The mean expression of interferon gamma mRNA was significantly higher in peripheral blood mononuclear cells than in gingival tissues. In contrast, the mean expression of IL-10 mRNA was higher in gingival tissues than in peripheral blood mononuclear cells. This high expression of IL-10 mRNA was, in fact, seen in only 7 gingival tissue samples with the majority of samples showing levels similar to peripheral blood mononuclear cells. There was no difference in the mean expression of IL-12 p35 mRNA between gingival tissues and peripheral blood mononuclear cells. However, IL-12 p40 mRNA was expressed higher in gingival tissues than in peripheral blood mononuclear cells in 6 out of 16 samples with significant difference of mean expression. Like IL-10, gingival tissue samples and peripheral blood mononuclear cells expressed similar levels of IL-12 p40 mRNA. There was no difference in the mean expression of IL-13 in gingival tissues and peripheral blood mononuclear cells. Nevertheless, more peripheral blood mononuclear cell samples demonstrated high IL-13 mRNA expression than gingival tissue samples. IL-4 mRNA was weak but detectable in 3 gingival tissue samples. These results support the concept that cytokines form complex networks in periodontitis lesions and that their overlapping and redundant effects should be taken into account when considering the pathology of inflammatory periodontal disease. Dichotomous expression of IL-10 and IL-12 p40 mRNA in the periodontal lesion may be associated with disease entity.
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PMID:Cytokine messenger RNA expression in chronic inflammatory periodontal disease. 946 81

B-1 cells are physically and functionally unique B cells that produce polyreactive natural antibody. This study examined the activation of B-1 cells in inflamed gingival tissue. Serum IgG antibodies to phosphorylcholine, E. coli LPS, DNA, and some commensal bacteria were examined in adult periodontitis patients and healthy subjects. In addition, the proportion of B-1a (CD20+CD5+) cells and the amount of IL-6 and IL-10 in the inflamed gingival tissues were examined. The serum levels of IgG antibodies to phosphorylcholine, E. coli LPS, and commensal bacteria were significantly higher in the adult periodontitis patients than the healthy subjects. The proportion of B-1a cells and the amount of IL-6 and IL-10 were significantly higher in the inflamed gingival tissues than in peripheral blood from the healthy subjects. These results suggest the activation of B-1 cells in the inflamed gingival tissue of adult periodontitis patients, and that B-1 cells may serve as the first line of defense by producing polyreactive antibodies to phosphorylcholine, LPS, and commensal bacteria.
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PMID:Presence of activated B-1 cells in chronic inflamed gingival tissue. 985 87

Porphyromonas gingivalis, a gram-negative, black-pigmented anaerobe, is among the microorganisms implicated in the etiology of adult periodontal disease. This bacterium possesses a number of factors, including hemagglutinins, of potential importance in virulence. Several hemagglutinin genes have been identified, cloned, and expressed in Escherichia coli. The purpose of this study was to characterize host responses to purified recombinant hemagglutinin B (rHag B), using the conventional Fischer rat as the experimental animal model. The effectiveness of immunization with rHag B on protection against experimental periodontal bone loss following infection with P. gingivalis was also evaluated. Groups of rats were immunized by the subcutaneous route with rHag B in complete Freund's adjuvant, immunized with rHag B and orally infected with P. gingivalis, nonimmunized and noninfected, or orally infected with P. gingivalis only. Serum and saliva samples were collected throughout the experiment and evaluated for serum immunoglobulin G (IgG) and IgM and salivary IgA antibody activity by enzyme-linked immunosorbent assay. No salivary IgA anti-Hag B activity was detected in the various groups of rats. A slight serum IgM response similar to that seen in preimmune samples was observed. Serum IgG antibody activity to Hag B was detected only in samples from rats immunized with rHag B. This response was primarily of the IgG1 and IgG2a subclasses, followed by IgG2b and low levels of IgG2c. Supernatants from rHag B-stimulated splenic lymphoid cell cultures from immunized rats contained high levels of gamma interferon, followed by interleukin-2 (IL-2), IL-10, and then IL-4. These results are consistent with the induction of T helper type 1 (Th1)- and Th2-like responses. Western blot analysis of sera derived from rHag B-immunized rats reacted with trichloroacetic acid (TCA) precipitates of P. gingivalis 33277, 381, A7A1-28, and W50, revealing a 50-kDa band reflective of Hag B. However, sera derived from rats immunized with P. gingivalis whole cells or from rats infected with P. gingivalis only did not react with rHag B but did react with TCA precipitates of P. gingivalis strains. Finally, radiographic measurements of periodontal bone loss indicated that rats immunized with rHag B had less bone loss than those infected with P. gingivalis only. These results demonstrate the effectiveness of purified rHag B in inducing a protective immune response and support the potential usefulness of this component of P. gingivalis in the development of a vaccine against adult periodontitis.
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PMID:Host responses to recombinant hemagglutinin B of Porphyromonas gingivalis in an experimental rat model. 1045 74

T-cell cytokine profiles in ten adult periodontitis and seven age-matched healthy or gingivitis subjects were determined. Porphyromonas gingivalis-specific T-cell lines were established from the peripheral blood of these individuals all of whom had past or present evidence of P. gingivalis infection. FACS analysis was used to determine the percentage of CD4- and CD8-positive cells in each line staining for cytoplasmic interleukin (IL)-4, interferon-gamma and IL-10. There were no differences in the mean percentage of IL-4-, interferon-gamma- or IL-10-positive T cells between the two groups. However, the individual profiles showed that the CD4 cells in five of the seven healthy or gingivitis lines had a higher proportion of interferon-gamma-positive cells, with two lines demonstrating higher percentages of IL-10- and/or IL-4-positive CD4 cells. Five of the ten adult periodontitis lines demonstrated either equal or higher percentages of IL-4-positive and/or IL-10-positive CD4 cells. With respect to the CD8 cells, two of the seven lines established from the healthy or gingivitis subjects and six of the ten adult periodontitis lines showed profiles with a higher percentage IL-4- and/or IL-10-positive cells. When the total T-cell contribution (CD4 plus CD8) for each T-cell line was determined from the individual CD4:CD8 ratios, only one of the healthy or gingivitis lines showed a profile with a higher proportion of IL-10-positive cells, while the results for the adult periodontitis lines were the same as indicated for the CD4 cell profiles, with five lines showing a higher percentage of IL-4- and/or IL-10-positive cells. In conclusion, this study has shown that in P. gingivalis-responsive T-cell lines established from adult periodontitis and healthy or gingivitis subjects, there was a predominant trend towards a higher percentage of interferon-gamma positive cells than either IL-4- or IL-10-positive cells. However, there were variations from this trend, although whether these variations indicate true susceptibility to progressive disease has yet to be determined.
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PMID:The proportion of interleukin-4, interferon-gamma and interleukin-10-positive cells in Porphyromonas gingivalis--specific T-cell lines established from P. gingivalis-positive subjects. 1055 Nov 52

To characterize the T cell response to Porphyromonas gingivalis, we examined the expression of costimulatory molecules on T cells derived from adult periodontitis patients with high serum antibody titre to P. gingivalis. The expression of CD28, CTLA-4, CD40 ligand (CD40L) on CD4+ T cells was analysed by flow cytometry. IL-10 and transforming growth factor-beta (TGF-beta) mRNA expression were determined by reverse transcription-polymerase chain reaction (RT-PCR) and subsequent image analysis. Peripheral blood mononuclear cells (PBMC) derived from periodontitis patients showed higher proliferative responses to P. gingivalis outer membrane (OM) than those from healthy controls (P < 0.05). The percentage of CTLA-4+ cells within CD4+ T cells of patients was significantly higher than that of healthy controls after P. gingivalis OM stimulation (33.0% versus 11.9%, P < 0.01). There was no significant difference in the percentages of CD28+ cells and CD40L+ cells, and the percentage of CD40L+ cells was low in both groups even after stimulation. Stimulation of PBMC with P. gingivalis OM induced significantly higher IL-10 mRNA expression in periodontitis patients than in healthy controls (P < 0.05). The level of TGF-beta mRNA expression of patients tended to be higher than that of healthy controls, but there was no significant difference. To elucidate the functional role of CTLA-4, we further investigated the secondary proliferative response to P. gingivalis OM. Interestingly, P. gingivalis OM stimulation did not enhance antigen-specific secondary response. Anti-CTLA-4 MoAb had no effect on proliferation in the presence of P. gingivalis OM. CTLA-4Ig suppressed the proliferative response significantly (P < 0.01). These results suggest that T cell responses to P. gingivalis OM may be regulated by CTLA-4 that is expressed at the late phase of T cell activation, and, in part, immunosuppressive cytokines. Taken together, CTLA-4 may play a crucial role in the pathogenesis of chronic inflammatory periodontal disease.
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PMID:Elevated CTLA-4 expression on CD4 T cells from periodontitis patients stimulated with Porphyromonas gingivalis outer membrane antigen. 1063 63

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