Literature DB >> 11207661

Anti-inflammatory cytokine IL-10 and T cell cytokine profile in periodontitis granulation tissue.

D F Lappin1, C P MacLeod, A Kerr, T Mitchell, D F Kinane.   

Abstract

Th2 cells are more abundant than Th1 cells in periodontitis lesions, but the relative importance of the Th1 and Th2 subsets in periodontal disease is not understood. In addition, the role of proinflammatory and anti-inflammatory cytokines in this disease process is unclear. Biopsies were obtained from 10 patients with early onset periodontitis (EOP) and 10 patients with adult periodontitis (AP). From all of the patients in the AP group we were able to obtain and section the gingival tissue to serve as controls. We used polyclonal monospecific antibodies to detect cells expressing IL-2, IL-4, IL-6, IL-10 and IL-15, tumour necrosis factor (TNF-alpha) and interferon-gamma (IFN-gamma) in formalin-fixed, paraffin-embedded sections of granulation tissue from periodontitis lesions. We also employed a series of oligonucleotide probes to detect cells expressing the cytokine transcripts in the same tissue biopsies. Cells that expressed IL-4 or IL-6 were more numerous than cells expressing either IL-2 or IFN-gamma. Th2 cells were more numerous in EOP and AP tissues. IL-15 substitutes for IL-2 in a number of biological activities related to the Th1 immune response, and interestingly, in periodontal lesions the IL-15-expressing cells outnumbered IL-2-expressing cells, suggesting that this is the pattern of immune regulation by T cells in the periodontium. The functional balance in the T cell subsets detected by their cytokine profiles underlies the importance of the anti-inflammatory mechanisms taking place in the diseased tissue. The numbers of inflammatory leucocytes that express the anti-inflammatory cytokine IL-10 are much more widely distributed than those that express the proinflammatory cytokines IL-6 and TNF-alpha. This study suggests that large numbers of infiltrating inflammatory cells as well as accessory cells are involved in the down-regulation of the inflammatory and immune response in periodontitis.

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Year:  2001        PMID: 11207661      PMCID: PMC1905981          DOI: 10.1046/j.1365-2249.2001.01448.x

Source DB:  PubMed          Journal:  Clin Exp Immunol        ISSN: 0009-9104            Impact factor:   4.330


  33 in total

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Authors:  J L Ebersole; M A Taubman
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Review 3.  Cytokines and prostaglandins in immune homeostasis and tissue destruction in periodontal disease.

Authors:  E Gemmell; R I Marshall; G J Seymour
Journal:  Periodontol 2000       Date:  1997-06       Impact factor: 7.589

4.  Crevicular fluid and serum IgG subclasses and corresponding mRNA expressing plasma cells in periodontitis lesions.

Authors:  D F Kinane; K Takahashi; J Mooney
Journal:  J Periodontal Res       Date:  1997-01       Impact factor: 4.419

5.  Possible role of T cells in the establishment of IgG plasma cell-rich periodontal lesion--augmentation of IgG synthesis in the polyclonal B cell activation response by autoreactive T cells.

Authors:  H Ito; Y Harada; T Matsuo; S Ebisu; H Okada
Journal:  J Periodontal Res       Date:  1988-01       Impact factor: 4.419

6.  T-cell requirement for establishment of the IgG-dominant B-cell lesion in periodontitis.

Authors:  H Okada; H Ito; Y Harada
Journal:  J Periodontal Res       Date:  1987-05       Impact factor: 4.419

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Authors:  H Okada; T Kida; H Yamagami
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8.  Humoral immune responses in periodontal disease may have mucosal and systemic immune features.

Authors:  D F Kinane; D F Lappin; O Koulouri; A Buckley
Journal:  Clin Exp Immunol       Date:  1999-03       Impact factor: 4.330

9.  Relative proportions of mononuclear cell types in periodontal lesions analyzed by immunohistochemistry.

Authors:  D F Lappin; O Koulouri; M Radvar; P Hodge; D F Kinane
Journal:  J Clin Periodontol       Date:  1999-03       Impact factor: 8.728

10.  Cytokine profiles of cells extracted from humans with periodontal diseases.

Authors:  E Gemmell; G J Seymour
Journal:  J Dent Res       Date:  1998-01       Impact factor: 6.116

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  30 in total

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Review 2.  Inflammatory and immune pathways in the pathogenesis of periodontal disease.

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Journal:  Periodontol 2000       Date:  2014-02       Impact factor: 7.589

3.  Macrophage Polarization Alters Postphagocytosis Survivability of the Commensal Streptococcus gordonii.

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4.  MyD88-mediated innate sensing by oral epithelial cells controls periodontal inflammation.

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5.  Capsaicin inhibits Porphyromonas gingivalis growth, biofilm formation, gingivomucosal inflammatory cytokine secretion, and in vitro osteoclastogenesis.

Authors:  Y Zhou; X Guan; W Zhu; Z Liu; X Wang; H Yu; H Wang
Journal:  Eur J Clin Microbiol Infect Dis       Date:  2013-08-17       Impact factor: 3.267

6.  Smoking-related cotinine levels and host responses in chronic periodontitis.

Authors:  J L Ebersole; M J Steffen; M V Thomas; M Al-Sabbagh
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7.  Th1 biased response to a novel Porphyromonas gingivalis protein aggravates bone resorption caused by this oral pathogen.

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Review 8.  The potential of p38 MAPK inhibitors to modulate periodontal infections.

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9.  Immunologic environment influences macrophage response to Porphyromonas gingivalis.

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10.  Influence of IL-6 haplotypes on clinical and inflammatory response in aggressive periodontitis.

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