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

IL-2, interferon-gamma (IFN-gamma), IL-4 and IL-6 producing T cells in periodontitis and gingivitis-affected human tissues were investigated by immunohistochemistry to clarify the relationship between T cell functional subsets and disease entity. Using alkaline-phosphatase anti-alkaline-phosphatase technique, the relative proportions of each cytokine-producing T cell were calculated in the crevicular 1/3, middle 1/3 and oral 1/3 areas selected in the connective tissue of sections. CD19:CD3 and CD4:CD8 ratios were determined on the serial sections. Compared with gingivitis tissues, the proportion of cytokine-producing cells in periodontitis-affected samples was higher overall in the crevicular 1/3 (P < 0.02). The middle 1/3 exhibited a higher percentage of cytokine-producing cells, except for IL-6-producing cells. Frequencies of cytokine-producing cells in the oral 1/3 did not differ. IL-4 was the prominent cytokine in periodontitis-affected tissues, with the highest proportion detected in the crevicular 1/3. The CD19:CD3 ratio was higher in periodontitis tissues irrespective of the location, indicating a B cell dominance in periodontitis lesions. Furthermore, a significant positive correlation between the proportion of IL-4-producing cells and the CD19:CD3 ratio was noted. The CD4:CD8 ratio consistently exceeded 2.0 in both periodontitis and gingivitis. These results suggest that immunoregulation of both periodontitis and gingivitis are T cell-dependent, but in periodontitis type 2 helper T cells predominate and thereby control B cell activation.
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PMID:Immunohistological analysis of T cell functional subsets in chronic inflammatory periodontal disease. 788 61

We have shown that gamma delta T cells in human gingiva have an intraepithelial location and, that in the chronic inflammatory disease periodontitis, the expression of CD45RO and CD8 or CD4 is induced on gamma delta T cells. To study the role of gamma delta T cells in local antibacterial responses, we determined the cytokine profiles of isolated human gingival cells. Different T cell subpopulations, isolated by positive selection with mAb-coated magnetic beads and macrophages, as well as epithelial cells, were analyzed for expression of mRNA for 15 cytokines by reverse transcriptase-PCR. The ultrastructure of gingival gamma delta T cells was also studied. The gamma delta T cells expressed mRNA for IFN-gamma, TNF-alpha, TGF-beta 1, and IL-6. Expression of IFN-gamma was a consequence of inflammation. CD4+ gamma delta T cells expressed IFN-gamma only, whereas CD8+ gamma delta T cells expressed all four cytokines. CD8+ cells expressing IFN-gamma, TNF-alpha, and IL-6 in combination suggest a cytotoxic effector function. Gingival gamma delta T cells contained cytoplasmic electron-dense membrane-bound granules and multivesicular bodies that are ultrastructural characteristics of cytotoxic cells. Epithelial cells from inflamed gingiva expressed HLA-DR, CD1a, CD1c, and heat shock protein 60 on the cell surface. They also expressed mRNA for IL-1 beta, IL-6, IL-8, TNF-alpha, and TGF-beta 1. Thus, epithelial cells may function as accessory cells in immune activation and, at the same time, be target cells for CD8+ gamma delta T cells reactive with CD1 Ag or heat shock protein. These results suggest that gamma delta T cells constitute a first line of defense in gingiva, preventing entrance of pathogens by cytotoxicity against infected and stressed epithelial cells, and by control of epithelial cell growth through secretion of regulatory cytokines.
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PMID:Cytokine profile and ultrastructure of intraepithelial gamma delta T cells in chronically inflamed human gingiva suggest a cytotoxic effector function. 805 26

Although patients with refractory periodontitis have been widely reported, no clear biologic profile of these patients has been noted. The purpose of the present study was to evaluate host responsiveness of a well-defined group of refractory periodontitis patients by determining the effect of a lipopolysaccharide (LPS) challenge on monocyte surface receptor density and on the release of inflammatory mediators. Venous blood was obtained from 7 refractory periodontitis, 8 stable periodontal maintenance, and 8 gingivitis patients with no evidence of periodontitis. Mononuclear cells were cultured in either control media or media treated with Actinobacillus actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), or Salmonella typhimurium (S. typh) LPS. At 0 and 24 hours supernatants were assayed for prostaglandin-E2 (PGE2) and interleukin-1 beta (Il-1 beta) release by ELISA. Using flow cytometry the density of specific monocyte surface receptors were assayed with Mo3e and LeuM3 monoclonal antibodies (mAb); T-cell CD4/CD8 ratios were assayed with OKT-3, OKT-4, and OKT-8 mAb. After 24 hours incubation with Pg or S. typh LPS, the upregulation of the Mo3e receptor was significantly decreased for refractory periodontitis patients (P < 0.05) when compared to gingivitis and to stable maintenance patients. In refractory periodontitis patients the T-cell CD4/CD8 ratio was decreased. Upon stimulation with Pg or S. typh LPS, monocytes from stable maintenance and refractory periodontitis patients released more Il-1 beta (P < 0.05) and PGE2 (P = 0.13 and 0.15) than monocytes from gingivitis subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Host responses in patients with generalized refractory periodontitis. 813 19

Expression of adhesion molecules, CD11a, CD11b and CD18, and of the function-associated molecules CD3, CD4, CD8, CD16, CD19, CD56 and CD57 was assayed on peripheral blood leukocytes from normal control subjects (n = 10), and from patients with adult periodontitis PD (n = 9), ankylosing spondylitis AS (n = 11) and rheumatoid arthritis RA (n = 14). A novel rapid fixation leukocyte preparation technique was used which prevents artefactual up-regulation of surface antigens. In RA patients, the percentage of CD18+ lymphocytes was decreased and that of CD11b+ neutrophils was increased. On lymphocytes the mean fluorescence intensity (MFI) of both CD11b and CD18 was decreased whereas that of CD57 was increased. In AS patients the percentages of CD11b+ lymphocytes and neutrophils were increased and CD18+ lymphocytes and neutrophils were decreased. On lymphocytes the MFIs of CD11b and CD18 were decreased, whilst that of CD16 was increased. On neutrophils the MFI for CD18 was increased. No significant differences (p < 0.01) were seen for the periodontitis patients. It is suggested that the antigen expression on peripheral blood cells from RA and AS patients is consistent with leukocyte activation.
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PMID:Leukocyte activation and function-associated antigens in inflammatory disease. 831 19

Activated T lymphocytes constitute a major component of inflammatory cells in the early periodontal lesion, and also appear in the gingival crevicular fluid. In an attempt to clarify the relationship between the ICAM-1 (CD54) expression of pocket epithelium in gingiva and the infiltrating lymphocyte population, we carried out an analysis of CD11a+(LFA-1 alpha), CD25+(IL-2R alpha) and CD4+(Th) cells subjacent to ICAM-1-expressing pocket epithelia and CD11a+CD25+CD4+ cells in gingival crevicular fluid (GCF). GCF was collected by crevicular washing from 16 patients with periodontitis (P group) and 3 subjects with healthy gingiva (H group). Peripheral blood (PB) was collected at the same time. Mononuclear cells were isolated by Ficoll-paque gradient centrifugation from GCF and PB. Monoclonal antibodies (mAb) to CD11a, CD25, and CD4 were used for three-color flow cytometry. Gingival biopsies were obtained from 7 patients in P group and 3 subjects in H group. Serial cryostat sections (6 microns in thickness) were prepared from each biopsy, on which a double staining was performed. The number of CD11a+CD25+CD4+ cells and the fluorescence intensity of FITC conjugated anti-CD11a were significantly higher in GCF than in PB (p < 0.001 to p < 0.01). CD11a+CD25+CD4+ cells were not detected in GCF in H group. The pocket epithelia expressed CD54 in P group, but not in H group. The number of CD11a+, CD25+ and CD4+ cells infiltrating the connective tissue subjacent to the upper, middle and lower parts of the CD54 positive pocket epithelium (n = 16) was 141 +/- 26, 38 +/- 13, 144 +/- 29 (cells/0.04 mm2), respectively, whereas in the CD54 negative pocket epithelium, it was (n = 5) 9 +/- 2, 3 +/- 1, 8 +/- 3. In P group, the CD11a+CD25+CD4+ cell number in GCF correlated with CD25+, CD11a+ cells in the connective tissue subjacent to the CD54+ pocket epithelium. These results indicate that expression of ICAM-1 in pocket epithelium is relevant to the migration of CD11a, CD25, CD4 positive cells in connective tissue subjacent to the pocket epithelium into the periodontal pocket. Assessing the relationship of our findings and other adhesion molecules would offer important clues to the understanding of T cell migration in affected gingiva.
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PMID:ICAM-1-expressing pocket epithelium, LFA-1-expressing T cells in gingival tissue and gingival crevicular fluid as features characterizing inflammatory cell invasion and exudation in adult periodontitis. 854 7

Inflamed gingival tissues are enriched in macrophages (MOs) and CD4-positive T cells; however, T helper-type cytokines such as interleukin (IL)-2 and IL-4 are absent. Therefore, we investigated whether a relationship exists between IL-4 receptor (IL-4R) expression and MO persistence in the absence of exogenous IL-4. Gingival MOs, when compared with monocyte(MN)/MOs from peripheral blood mononuclear cells, expressed high levels of IL-4R mRNA. Furthermore, in vitro cultures of gingival MOs remained viable whereas identically treated peripheral blood MN/MOs rapidly lost viability. However, when gingival MOs were incubated with recombinant IL-4 (rIL-4), the cell viability was dramatically reduced. When the frequency of apoptotic cells was assessed in rIL-4-treated gingival MO cultures, higher numbers of apoptotic cells were noted in rIL-4-treated versus control cultures. Furthermore, rIL-4-treated MOs from inflamed gingiva showed DNA fragmentation as assessed by electrophoresis. These findings clearly show that addition of exogenous rIL-4 to gingival MO cultures leads to cell death by apoptosis. This finding would suggest that topical application of rIL-4 may inhibit the persistence of MOs in adult periodontitis, which could then lead to decreased inflammation.
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PMID:Absence of exogenous interleukin-4-induced apoptosis of gingival macrophages may contribute to chronic inflammation in periodontal diseases. 854 23

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

Porphyromonas gingivalis plays a major role in the pathogenesis of periodontal disease, however some individuals with P. gingivalis infection do not experience periodontal breakdown. The aim of this study was to investigate the proliferative responses of two highly defined groups of subjects and to establish and characterize peripheral blood and gingival cell T cell lines and clones from subjects from these groups. The two groups were selected on the basis of P. gingivalis in their plaque and the presence of serum anti-P. gingivalis antibodies. Both groups therefore were seen to have P. gingivalis and to have responded to it. They however differed only in their clinical susceptibility (adult periodontitis) or resistance (gingivitis) to periodontal breakdown. Dose responses of peripheral blood mononuclear cells extracted from the subjects showed a trend towards a lower response by the adult periodontitis group to P. gingivalis outer membrane (OM) antigens. Peripheral blood T cell lines and clones responsive to P. gingivalis OM were established from a high responding gingivitis subject and a low responding adult periodontitis subject. Gingival T cell lines and clones were also derived from cells extracted from the periodontal tissues of the same periodontitis subject. The majority of T cells in the peripheral blood T cell line from the gingivitis subject were CD4 while those from the adult periodontitis subject were CD8. The gingival T cell line was CD3+ve CD4-ve and CD8-ve. All lines and clones proliferated slowly to P. gingivalis OM but phytohaemagglutinin (PHA) induced an increase in DNA synthesis in those derived from the gingivitis subject with little to no effect on those established from the adult periodontitis subject. Furthermore, PHA inhibited the proliferative response of the CD8 clone derived from the adult periodontitis subject. Phenotypic analysis demonstrated that all the peripheral blood clones expressed the alpha beta TCR while the gingival T cell clones expressed the gamma-delta TCR. All clones had the memory/primed CD45RO+ve phenotype and at least 80% of cells in each clone were HLA-DR+ve. A lower percent of gingival cells expressed CD45RA than the CD4 peripheral blood clones and the two CD8 clones also had a decreased CD45RA expression. The gingival T cell clones also expressed a low percent CD25 as did the CD8 clone derived from the adult periodontitis subject. The results suggest that clones derived from the gingivitis and adult periodontitis subject may be functionally different. The presence of gamma-delta T cells in adult periodontitis remains to be confirmed and their function determined.
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PMID:Characterization of T lymphocyte clones derived from Porphyromonas gingivalis infected subjects. 863 76

T cells are central to the immune response to infection and studies have indicated a local immunoregulatory imbalance may exist in human periodontal disease. Since Porphyromonas gingivalis is generally recognized as a major periodontopathogen, the aim of this study was to establish T cell lines and clones specific to P. gingivalis from the gingival tissues and peripheral blood of P. gingivalis--infected subjects. Two subjects were selected from two groups of individuals (one from each group) established on the basis of P. gingivalis in their plaque and the presence of serum antibodies which react with P. gingivalis antigens. The two groups differed however in their clinical susceptibility (adult periodontitis) or resistance (gingivitis) to periodontal breakdown. The mean ages +/- standard error of the mean of the two groups were 47.9 +/- 2.2 and 49.6 +/- 3.7, respectively, so that resistance in the gingivitis group was related to the age of the subjects. T cell lines and clones were established from the peripheral blood of one patient from each of the two groups and also from the gingival tissues of the same periodontitis subject. This study has demonstrated the capability of establishing P. gingivalis-specific T cell lines and clones from P. gingivalis-infected subjects and FACS analysis of the T cell receptor variable regions demonstrated that the clones were indeed monoclonal. The CD4:CD8 ratios of the peripheral blood-derived T cell lines were 1.2 and 0.4 for the gingivitis-derived line and the periodontitis-derived line, respectively, thus supporting the clinical differences displayed by the two subjects.
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PMID:Establishment of peripheral blood and gingival T lymphocyte clones responsive to Porphyromonas gingivalis. 867 31

This study was performed to determine the type of periodontal pathology found in a group of HIV+ patients and its relation to serum levels of CD4. The sample consisted of 101 individuals: intravenous drug users (84%), homosexuals (7%), and heterosexuals (10%). Each patient was examined clinically and radiographically. Periodontal clinical parameters included gingival index and probing depth and loss of attachment on four sites per tooth. Severity of disease was defined as the most severe lesion found: gingivitis, or early, moderate, or advanced periodontitis. CD4 counts were determined on 64 of these patients. Associations between severity of the disease and gender and CD4 counts were analyzed using the Mantel Haenszel chi square test, while associations between severity and age and CD4/CD8 ratio were analyzed using the Kruskal-Wallis test. No disease was found in 14.8% of the sample, gingivitis was found in 21.8%, early periodontitis in 43.6%, moderate periodontitis in 10.9%, and advanced periodontitis in 8.9%. Linear gingival erythema (LGE) was seen in 17.8% of all patients and necrotizing periodontitis (NUP) in 4.9%. No statistically significant differences were observed between the severity of the disease and CD4 counts.
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PMID:Periodontal disease in HIV seropositive patients and its relation to lymphocyte subsets. 867 70


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