Effect of periodontal treatment on the serum antibody levels to heat shock proteins

Yamazaki, Kazuhisa; Ueki-Maruayama, K.; Honda, Takeshi; Nakajima, Takako Eguchi; Seymour, G. J.

doi:10.1111/j.1365-2249.2003.02375.x

Cited by 31 publications

(32 citation statements)

References 28 publications

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“…If left untreated, periodontitis may culminate in tooth loss. Elevated levels of P. gingivalis are detected in periodontal lesions, and these can be significantly reduced following successful periodontal therapy (Cappelli et al, 2009;Salvi et al, 1997;Socransky et al, 2002;Ximenez-Fyvie et al, 2000;Yamazaki et al, 2004). Apart from its well accepted role as an oral pathogen in the establishment of chronic inflammation at the site of infection, there is increasing evidence of a link between P. gingivalis-associated periodontal disease and systemic inflammatory conditions, such as diabetes, preterm birth, aspiration pneumonia and atherosclerotic cardiovascular disease (Brodala et al, 2005;Liao et al, 2009;Lin et al, 2003;Maekawa et al, 2011;Pussinen and Mattila, 2004).…”

Section: Introductionmentioning

confidence: 99%

Involvement of the TREM-1/DAP12 pathway in the innate immune responses to Porphyromonas gingivalis

Bostancı

Thurnheer

Belibasakis

2011

Molecular Immunology

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Porphyromonas gingivalis, is a Gram-negative obligate oral anaerobic bacterium highly implicated in periodontal disease, the most prevalent chronic inflammatory disease, but recent evidence also indicates a potential contribution to systemic inflammation. The Triggering Receptor Expressed on Myeloid cells 1 (TREM-1) is a cell surface receptor of the immunoglobulin superfamily, which, along with its adaptor signalling molecule DAP12, is involved in immune response to bacterial and fungal infections, particularly by amplifying the production of pro-inflammatory cytokines by the host. The aim of the present study was to investigate the effect of P. gingivalis on the expression of the TREM-1/DAP12 pathway, as well as its engagement in pro-inflammatory cytokine production, by the myelomonocytic cell line MonoMac-6. P. gingivalis enhanced TREM-1 gene expression by the cells, concomitantly to an increase of soluble TREM-1 secretion. Engagement of TREM-1, by introducing anti-TREM-1 to the experimental system, resulted in further potentiation of the pro-inflammatory responses to P. gingivalis, as evaluated by a further enhancement of interleukin (IL)-1 and IL-6 secretion. On the contrary, the synthetic TREM-1 antagonist LP17 reduced the P. gingivalis-induced IL-1 and IL-6 secretion by approximately 50%. In conclusion, the putative periodontal pathogen P. gingivalis can positively regulate the expression of the TREM-1/DAP12 pathway in monocytic cells. Moreover, engagement of TREM-1 can further potentiate the pro-inflammatory responses to P. gingivalis infection. This effect may contribute not only to the pathogenesis of inflammatory periodontal disease, but also to the enhancement of systemic inflammation.

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Section: Introductionmentioning

confidence: 99%

Involvement of the TREM-1/DAP12 pathway in the innate immune responses to Porphyromonas gingivalis

Bostancı

Thurnheer

Belibasakis

2011

Molecular Immunology

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“…Although there are many studies exploring the role of PD as a chronic infection with implications for several systemic diseases (Ishikawa et al, 1997;Yamazaki et al), there is a lack of studies on chronic pain due to PD. Therefore, studies of this kind are important for managing these chronic disorders, which are very prevalent.…”

Section: Discussionmentioning

confidence: 99%

“…It is chronic and usually painless, except in some cases when provoked by a mechanical stimulus (chewing or teeth brushing) or during an acute episode (Brunsvold & Prakash, 1999). Considering the presence of inflammation and the rich nerve supply in the gingival tissue, PD stimulates both immune system and pain pathways (Yamazaki et al, 2004). The association of PD with some systemic conditions such as cardiovascular, metabolic and neurovascular diseases has been previously demonstrated (Amar et al, 2003;Fabri et al, 2009).…”

Section: Introductionmentioning

confidence: 97%

The Expression of Nitric Oxide in the Gingival Tissue in Subjects with Periodontitis and Chronic Pain

Fabri¹,

Sannomiya²,

Prado

et al. 2014

Int. J. Odontostomat.

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Periodontal disease (PD) is a chronic infection that may have local and systemic rebound. Although a series of inflammatory mediators are involved in PD, the mechanisms involved in chronic craniofacial pain associated with it require elucidation. The aim of this study was to evaluate the immunoreactivity of substance P (SP), neuronal (nNOS) and inducible (iNOS) nitric oxide synthases in gingival samples of patients with severe PD with and without chronic craniofacial pain. Gingival specimens were obtained during routine periodontal surgery while managing 20 patients with both PD and chronic craniofacial pain (CFP Group) and 18 patients with only PD (PD Group). Following surgical removal, the tissue underwent routine histological techniques and was stained by immunohistochemistry with antibodies against SP, nNOS and iNOS. Using an image analysis system, we assessed the SP, nNOS and iNOS content in total gingival tissue as well as in both epithelial and connective gingival area. We observed high expression of nNOS in gingival tissue obtained from CFP patients (p<0.001), particularly in the epithelium area (p<0.001) comparatively to PD patients. In addition, the iNOS expression was also increased in the CFP group in the connective gingival tissue (p=0.003). There was no difference concerning SP expression between the groups. Our results suggest that nitric oxide, particularly derived from nNOS, modulates not only PD but also chronic craniofacial pain, since patients with this association presented an increase in nNOS and iNOS expression in gingival tissue.

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“…Younger aged patients with advanced periodontitis may represent a different diagnostic category or a different spectrum of response from older patients suffering from chronic periodontitis [14], and may mount different immune responses [15]. The recruitment of patients who are undergoing treatment for chronic periodontitis [5] is problematic and may yield conflicting results as treatment of CP has a modulating effect on humoral immune responses to HSP [16] and instrumentation may immunise patients with plaque antigens. To minimise the confounding effect of treatment in our results we recruited untreated cases.…”

Section: Discussionmentioning

confidence: 99%

Immune Responses to HSP65/60 in Periodontal Disease

Hasan¹,

Foo²,

Sadoh³

et al. 2012

JIBTVA

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Chronic periodontitis (CP) is a chronic inflammatory condition which destroys the supporting tissues of teeth and increases in prevalence with age. Immune responses against heat shock proteins (HSP) can be cross-reactive among bacterial and human antigens. There is evidence that microbial HSP65 and human HSP60 are involved in periodontal disease. The aim of this study is to investigate immune responses to the human HSP60 and microbial HSP65 in patients with CP and relate these to the level of inflammation and smoking status. We collected serum samples from 30 patients with chronic gingivitis (CG) and 30 patients with CP. In each group, eight subjects were current smokers. ELISA was used to determine the levels of serum anti-HSP and C-reactive protein (CRP) in each group. Peripheral blood mononuclear cells were also isolated and stimulated with HSPs. Significant lymphoproliferation was seen in CP when stimulated with human HSP60. CRP and serum anti-human HSP60 IgG were elevated in CP compared to the CG, but not serum anti-microbial HSP 65 IgG. In view of the potential confounding effects of smoking in CP, a group of current smokers (n = 16) was also recruited to investigate whether smoking affects HSP immune responses. There was no significant difference in HSP-induced lymphoproliferation between smokers and non-smokers in either the CG or CP. There was a significant correlation between CRP and lymphoproliferative responses to Human HSP60 irrespective of smoking status. This study shows that serum anti-human HSP60 IgG and serum CRP are raised in untreated CP. In CP, serum CRP levels correlated significantly with human HSP60-induced lymphoproliferation, but not with anti-HSP antibody levels.

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Effect of periodontal treatment on the serum antibody levels to heat shock proteins

Cited by 31 publications

References 28 publications

Involvement of the TREM-1/DAP12 pathway in the innate immune responses to Porphyromonas gingivalis

Involvement of the TREM-1/DAP12 pathway in the innate immune responses to Porphyromonas gingivalis

The Expression of Nitric Oxide in the Gingival Tissue in Subjects with Periodontitis and Chronic Pain

Immune Responses to HSP65/60 in Periodontal Disease

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