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)

Immunological mechanisms participate in the pathogenesis of human chronic inflammatory periodontal disease (CIPD). Human CD4(+) lymphocytes express functionally heterogeneous profiles of cytokine production. CD26 is an integral membrane glycoprotein, that is, a marker of Th1-like cytokine development. The purpose of the present study was to compare the immuno-expression of CD26 receptor in periodontal sites with and without clinical attachment loss (CAL). Five patients with rapidly progressing periodontitis and one with juvenile periodontitis were investigated. Each patient presented at least one site with and without CAL. Ten sites with CAL and nine without any CAL were biopsied, followed by the immunohistochemical identification of the CD26 receptor using the MIB-DS2/7 antibody. The results demonstrated that the percentage of positive cells for this antigen in the periodontal sites with CAL was not significantly different from those without attachment loss. Therefore, Th1 cell impairment may not be directly involved with periodontal attachment loss.
 ...
PMID:CD26 Immuno-Expression and Periodontal Disease Progression. 1248 16

The aim of the present study was evaluation the distribution of B- and T-cells and T-cell subsets in periodontal tissues from patients with different periodontitis forms. Periodontal tissue samples were collected from group P patients during routine surgical procedures, while from group C during tooth extraction for orthodontic or prosthetic purposes. Directly after collection, tissue samples were placed in a criostat or fixed in 10% buffered formalin for 24 h at room temperature. Following fixation the material was embedded in paraffin and subjected to routine histological techniques. Examinations of B- and T-lymphocytes populations and T-lymphocytes subsets were made with the use of immunohistochemical method. In C group single T and B lymphocytes were found in histological examination in pocket epithelium zones. In early onset periodontitis (EOP) patients in inflammatory infiltration lymphocytes T were dominating while in adult periodontitis (AP) patients dominating were B lymphocytes. Mean CD4/CD8 ratio in control group was 1.7 and in EOP and AP patients 1.1 and 2.6 respectively.
 ...
PMID:Evaluation of lymphocyte populations and subpopulations extracted from inflamed periodontal tissues. 1253 63

To study anti-bacterial immunity and to identify critical bacterial antigens associated with specific periodontal infection, we screened the genomic library of Actinobacillus actinomycetemcomitans, a major Gram(-) anaerobe causing human periodontitis, by expression cloning using disease-associated periodontal CD4(+)T cells derived from HuPBL-engrafted NOD/SCID mice. Here, we report one of the novel genes identified and designated, cagE homologue (in short: cagE) of A. actinomycetemcomitans, which encodes a putative bacterial type IV secretion system with significant homology to Helicobacter pylori CagE and Agrobacterium tumefaciens VirB4. All serum samples from A. actinomycetemcomitans-infected periodontitis patients, but not from the healthy controls, readily recognized CagE by ELISA and Western blot, suggesting its biological and clinical significance. The CagE protein, upon secretion, elicited significant apoptosis on primary human epithelia, endothelia, osteoblasts, and T cells by 4-12h in vitro. Importantly, both cagE(-) mutant strain and N-terminus truncated CagE protein drastically reduced (p<0.001) the induction of apoptosis on human epithelia in vitro. These data strongly suggest that a novel effector protein, CagE in A. actinomycetemcomitans, induces apoptosis of human cells and destructive immunity, thereby it may play an important role in the pathogenesis of A. actinomycetemcomitans-mediated infections.
 ...
PMID:Expression cloning of a periodontitis-associated apoptotic effector, cagE homologue, in Actinobacillus actinomycetemcomitans. 1268 47

Oral manifestations were studied in 87 HIV-positive Thai adults (study 1), 45 HIV-positive children (study 2) and 101 HIV-positive (study 3). In study 1, 48% of patients had oral lesions; 23% had one and 13.8% two oral manifestations. Oral pseudomembranous candidiasis was found in 10.3%, erythematous candidiasis in 6.9%, and hairy leukoplakia (HL) in 11.5% of the patients. In study 2, 24.4% of children revealed one, 17.8% two and 6.6% three oral lesions; erythematous candidiasis was seen in 17.8%, and HL in 6.7% of the children. Fifteen patients (33.3%) received antiretroviral therapy. In study 3, pseudomembranous candidiasis was found in 52.5%, HL in 35.6% and necrotizing gingivo-periodontitis in 27.7%. Only 10% of patients were without oral lesions. The present three studies among HIV-infected Thai and Cambodians indicated a high prevalence of oral lesions, particularly variants of oral candidiasis such as pseudomembranous and erythematous candidiasis. Also, oral HL was a common finding, more so in patients with AIDS-associated diseases as represented by patients of study 3. Oral candidiasis and oral HL also seem to be quite prevalent in pediatric HIV-infected patients. In the absence of parameters indicating the degree of immunosuppression (CD4(+) cell counts and viral load) these oral lesions may be considered strong indicators of HIV-associated immunodeficiency.
 ...
PMID:Oral manifestations in HIV-infected individuals from Thailand and Cambodia. 1292 May 91

Gingival epithelium is a site of active trafficking of Langerhans cells (LCs), while the lamina propria in chronic periodontitis (CP) contains CD83+ mature dendritic cells (mDCs) and CD4+ T-cells. The immune cells that contribute to the mDCs, and whether mDCs engage with T-cells in situ, are unclear. Using several immunohistochemical approaches, combined with fluorescence-, light-, and scanning laser confocal-microscopy, we show that, in addition to LCs, the gingiva contains dermal DCs (DDCs) in the lamina propria; moreover, DDCs increase in number during CP. Furthermore, DDCs, LCs, and B-cells co-express CD83 in CP and contribute to the mDC pool. Double-staining for CD83 and CD4 revealed that mDCs associate with clusters of CD4+ T-cells in the lamina propria. Analysis of these data suggests that multiple DC subsets mature in the gingiva and that mature DCs engage in antigen presentation with T-cells in chronic periodontitis.
 ...
PMID:Multiple dendritic cell (DC) subpopulations in human gingiva and association of mature DCs with CD4+ T-cells in situ. 1293 60

Gingipains are trypsin-like cysteine proteinases produced by Porphyromonas gingivalis, a major causative bacterium of adult periodontitis. Rgps (HRgpA and RgpB) and Kgp are specific for -Arg-Xaa- and -Lys-Xaa- peptide bonds, respectively. HRgpA and Kgp are non-covalent complexes containing separate catalytic and adhesion/hemagglutinin domains, while RgpB has only a catalytic domain with a primary structure essentially identical to that of the cata-lytic subunit of HRgpA. The multiple virulence activities of gingipains are reviewed in view of the biphasic mechanisms: activation and inactivation of host proteins. Rgps enhanced vascular permeability through prekallikrein activation or direct bradykinin release in combination with Kgp. This Rgp action is potentially associated with gingival edema and crevicular fluid production. Rgps activate the blood coagulation system, leading to progression of inflammation and consequent alveolar bone loss in the periodontitis site. Rgps also activate protease-activated receptors and induce platelet aggregation, which, together with the coagulation-inducing activity, may explain an emerging link between periodontitis and cardiovascular disease. Kgp is the most potent fibrinogen/fibrin degrading enzyme of the three gingipains in human plasma, being involved in the bleeding tendency at the diseased gingiva. Gingipains stimulate expression of matrix metalloproteinases (MMPs) in fibroblasts and activate secreted latent MMPs that can destroy periodontal tissues. Gingipains degrade cytokines, components of the complement system and several receptors, including macrophage CD14, T cell CD4 and CD8, thus perturbing the host-defense systems and thereby facilitating sustained colonization of P. gingivalis. Gingipains are potent virulence factors of P. gingivalis, and in many regards their pathogenic activities constitute new mechanisms of bacterial virulence.
 ...
PMID:The biphasic virulence activities of gingipains: activation and inactivation of host proteins. 1468 29

Porphyromonas gingivalis is a fimbriated mucosal pathogen implicated in chronic periodontitis (CP). The fimbriae are required for invasion of the gingival mucosa and for induction of CP in animal models of periodontitis. CP is associated with infection of immature dendritic cells (DCs) by P. gingivalis in situ and with increased numbers of dermal DCs (DDCs) and mature DCs in the lamina propria. The role of fimbriae in gaining entry into human DCs and how this modulates the inflammatory and effector immune responses, however, have not been explored. To address this, we generated monocyte-derived DCs (MDDCs) in vitro which phenotypically and functionally resemble DDCs. We show here that virulent fimbriated P. gingivalis 381, in contrast to its fimbria-deficient mutant, P. gingivalis DPG3, efficiently gains entry to MDDCs in a manner dependent on active cell metabolism and cytoskeletal rearrangement. In addition, uptake of 381, unlike DPG3, induces DCs to undergo maturation, upregulate costimulatory molecules, and secrete inflammation cytokines interleukin-1beta (IL-1beta), IL-6, tumor necrosis factor alpha, IL-10, and IL-12. Moreover, MDDCs pulsed with 381 also stimulated a higher autologous mixed lymphocyte reaction and induced a Th1-type response, with gamma interferon (IFN-gamma) being the main cytokine. Monocytes used as controls demonstrated fimbria-dependent uptake of 381 as well but produced low levels of inflammatory cytokines compared to MDDCs. When MDDCs were pulsed with recombinant fimbrillin of P. gingivalis (10 micro g/ml), maturation of MDDCs was also induced; moreover, matured MDDCs induced proliferation of autologous CD4(+) T cells and release of IFN-gamma. Thus, these results establish the significance of P. gingivalis fimbriae in the uptake of P. gingivalis by MDDCs and in induction of immunostimulatory Th1 responses.
 ...
PMID:Fimbriated Porphyromonas gingivalis is more efficient than fimbria-deficient P. gingivalis in entering human dendritic cells in vitro and induces an inflammatory Th1 effector response. 1497 81

A potent virulence factor, cagE homologue of Actinobacillus actinomycetemcomitans, was identified via an expression cloning strategy and periodontitis-associated CD4(+)T-cells of a humanized mouse model. Through the immuno-gold labeling with transmission electron microscopy, immunofluorescent staining, in vitro co-cultures and Western blot studies, the resulting data clearly demonstrate that: (i) in CagE-homologue treated human epithelia in vitro, there are ultra-structural features of plasma membrane blebbing, sub-cellular disorganization with condensed and marginalized chromatins along the nuclear membrane, consistent with the pro-apoptotic characteristics, (ii) the disturbed membrane integrity detected above is associated with localization of the CagE proteins on target cell surface, and (iii) CagE-homologue is located in the cytoplasm of A. actinomycetemcomitans and associated with a bacterial type-IV secretion system (T4SS), suggesting that its translocation is required for secretion. Thus, CagE-homologue may be critically involved in A. actinomycetemcomitans-induced tissue destruction, inflammation and subsequent adverse immunity in periodontal pathogenesis.
 ...
PMID:Apoptotic activity and sub-cellular localization of a T4SS-associated CagE-homologue in Actinobacillus actinomycetemcomitans. 1574 14

Recent studies have shown the biological and clinical significance of signaling pathways of osteogenic cytokines RANKL-RANK/OPG in controlling osteoclastogenesis associated with bone pathologies, including rheumatoid arthritis, osteoporosis, and other osteolytic disorders. In contrast to the inhibitory effect of gamma interferon (IFN-gamma) on RANKL-mediated osteoclastogenesis reported recently, alternative new evidence is demonstrated via studies of experimental periodontitis using humanized NOD/SCID and diabetic NOD mice and clinical human T-cell isolates from diseased periodontal tissues, where the presence of increasing IFN-gamma is clearly associated with (i) enhanced Actinobacillus actinomycetemcomitans-specific RANKL-expressing CD4(+) Th cell-mediated alveolar bone loss during the progression of periodontal disease and (ii) a concomitant and significantly increased coexpression of IFN-gamma in RANKL(+) CD4(+) Th cells. Therefore, there are more complex networks in regulating RANKL-RANK/OPG signaling pathways for osteoclastogenesis in vivo than have been suggested to date.
 ...
PMID:Gamma interferon positively modulates Actinobacillus actinomycetemcomitans-specific RANKL+ CD4+ Th-cell-mediated alveolar bone destruction in vivo. 1590 74

CD4+CD25+ regulatory T (Tr) cells are critical in regulating the immune response and thereby play an important role in the defense against infection and control of autoimmune diseases. Our previous studies demonstrated the involvement of autoimmune responses in periodontitis. The aim of this study was to identify CD4+CD25+ Tr cells in periodontitis tissues and compare them with those in gingivitis tissues. Immunohistological analysis of CD4, CD25, and CTLA-4 and the gene expression analysis of FOXP3, TGF-beta1, and IL-10 on gingival biopsies revealed the presence of CD4+CD25+ Tr cells in all tissues. In periodontitis, the percentage of CD4+CD25+ Tr cells increased with increasing proportions of B-cells relative to T-cells. FOXP3, a characteristic marker for CD4+CD25+ Tr cells, TGF-beta1 and IL-10 were expressed more highly in periodontitis compared with gingivitis. These findings suggest that CD4+CD25+ Tr cells and possibly other regulatory T-cell populations do exist and may play regulatory roles in periodontal diseases.
 ...
PMID:Regulatory T-cells infiltrate periodontal disease tissues. 1597 93


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>