Biomedical subjects

G J Seymour

Publications and source records attributed to G J Seymour.

At least 19 recordsLinked to original sources

PubMed2007

Anti-P. gingivalis response correlates with atherosclerosis.

Significant associations between atherosclerosis and both Porphyromonas gingivalis, a major periodontopathogen, and the respiratory pathogen, Chlamydia pneumoniae, have been shown. Many individuals with evidence of atherosclerosis demonstrate seropositivity to these pathogens. The aim of the present study was to examine the atherogenic effect of repeated immunizations with either or both of these agents, and to determine if molecular mimicry of bacterial heat-shock protein (HSP), termed GroEL, and host (h) HSP60 was involved. Atherogenesis was examined in apolipoprotein-E-deficient (-/-) mice following intraperitoneal immunizations with P. gingivalis, C. pneumoniae, P. gingivalis, and C. pneumoniae or vehicle. Lesion area in the proximal aorta and levels of serum antibodies to P. gingivalis, C. pneumoniae, and GroEL were measured. The increased pathogen burden of P. gingivalis, but not of C. pneumoniae, enhanced atherosclerosis. hHSP60 was detected in lesions, and in P. gingivalis-immunized mice, lesion development was correlated with anti-GroEL antibody levels, supporting the involvement of molecular mimicry between GroEL and hHSP60.

Animals↗

PubMed2006

Prostaglandin E2 enhances transforming growth factor-beta 1 and TGF-beta receptors synthesis: an in vivo and in vitro study.

The aims of this study were to determine how Prostaglandin E2 (PGE2) locally applied affected the immunodistribution of latent transforming growth factor-beta 1 (TGF-beta1), and how the eicosanoid modified TGF-beta1 release and TGF-beta receptors gene expression in cultured osteoblasts. PGE2 locally delivered on the rat mandible at doses of 0.1 and 0.05 mg/day, but not 0.025 mg/day, over 20 days significantly increased latent TGF-beta1 immunodistribution (P<0.001), comparing with a placebo-treated group. Cultured osteoblasts stimulated with 10(-5) or 10(-7)M PGE2 significantly varied the level of activated TGF-beta1 released into supernatants at different experimental periods compared with negative and positive controls. TGF-beta receptor type I gene expression was significantly increased in osteoblasts (P<0.01) after 10 days of treatment with 10(-5) and 10(-7)M PGE2, whereas 10(-3) M PGE2 produced the opposite effect. It is concluded that PGE2 may stimulate bone deposition by affecting TGF-beta pathway. This effect on the pathway appears to be dose-dependent.

Activin Receptors, Type I↗

PubMed2006

Arginase activity in a murine macrophage cell line (RAW264.7) stimulated with lipopolysaccharide from Actinobacillus actinomycetemcomitans.

AIMS: The aim of the present study was to determine whether or not lipopolysaccharide from Actinobacillus actinomycetemcomitans could stimulate arginase activity in a murine macrophage cell line (RAW264.7 cells). METHODS: RAW264.7 cells were treated with A. actinomycetemcomitans-lipopolysaccharide or lipopolysaccharide from Escherichia coli for 24 h. The effect of polymyxin B, l-norvaline, dl-norvaline, dexamethasone and cytokines (interferon-gamma and interleukin-4) on arginase activity in A. actinomycetemcomitans-lipopolysaccharide-stimulated cells was also determined. The cells were pretreated with anti-CD14, anti -toll-like receptor 2, or anti-toll-like receptor 4 antibody prior to stimulation with A. actinomycetemcomitans-lipopolysaccharide. Arginase activity was determined by a colorimetric assay. RESULTS: A. actinomycetemcomitans-lipopolysaccharide stimulated arginase activity in RAW264.7 cells in a dose-dependent manner, but was less potent than E. coli-lipopolysaccharide. Polymyxin B and l-norvaline, but not dl-norvaline, blocked the arginase activity in A. actinomycetemcomitans-lipopolysaccharide-stimulated cells. Dexamethasone and interleukin-4 but not interferon-gamma augmented arginase activity in A. actinomycetemcomitans-lipopolysaccharide-stimulated cells. Treatment of the cells with anti-CD14 and anti-toll-like receptor 4 but not anti-toll-like receptor 2 antibody decreased arginase activity in A. actinomycetemcomitans-lipopolysaccharide-stimulated cells. CONCLUSION: The results of the present study suggest that lipopolysaccharide from A. actinomycetemcomitans via CD14/toll-like receptor 4 complex molecules and the regulatory control of glucocorticoid and cytokines may stimulate arginase activity in RAW264.7 cells.

Aggregatibacter actinomycetemcomitans↗

PubMed2006

Role of CD4 and CD8 T-cells in the induction of oral tolerance to Actinomyces viscosus in mice.

Mucosal presentation of Actinomyces viscosus results in the induction of antigen specific systemic suppressor cells in mice. The aim of the present study was to determine the phenotype of the suppressor cells responsible for the induction of oral tolerance to low doses of A. viscosus. When CD8 cell-depleted DBA/2 mice were intragastrically immunized and systemically immunized with A. viscosus, the delayed type hypersensitivity response was suppressed but not the levels of antigen specific serum antibodies. Adoptive transfer of orally tolerized CD4(+) cells to CD4(+)-depleted mice resulted in suppression of delayed type hypersensitivity response but not of the levels of antigen specific serum antibodies. In contrast, adoptive transfer of orally immunized CD8(+) cells to CD8(+)-depleted mice resulted in partially suppressed delayed type hypersensitivity response but significantly inhibited the levels of antigen specific serum antibodies. When orally tolerized CD8(+) cells were cocultured with systemically immunized CD8(+) cell-depleted spleen cells, splenic specific antibodies were inhibited. However, no suppression of splenic specific antibodies could be observed in the cultures containing orally tolerized CD4(+) cells and systemically immunized CD4(+) cell-depleted spleen cells. The results of the present study suggest that oral tolerance of humoral and cellular immunity induced by low doses of A. viscosus may be mediated by CD8(+) and CD4(+) cells, respectively.

Actinomyces viscosus↗

PubMed2006

Inflammation, heat shock proteins and periodontal pathogens in atherosclerosis: an immunohistologic study.

BACKGROUND: Inflammation is a significant component of atherosclerosis lesions. Bacteria, including periodontopathogens, have been demonstrated in atherosclerotic plaques and cross-reactivity of the immune response to bacterial GroEL with human heat shock protein 60 has been suggested as a link between infections and atherosclerosis. METHODS: In this study, the nature of the inflammatory infiltrate and the presence of human heat shock protein 60 and GroEL were examined in 31 carotid endarterectomy specimens. Additionally, monoclonal antibodies were used to detect the presence of six bacteria, including those implicated in periodontal disease. RESULTS: The inflammatory cell infiltrate of the lesions was dominated by CD14(+) macrophages and CD4(+) T cells. Most cells of the infiltrate as well as the endothelium were HLA-DR(+), indicating activation; however, there was an absence of CD25 expression, demonstrating that the activated T cells were not proliferating. Few CD1a(+) and CD83(+) cells were noted. Human heat shock protein 60 expression was evident on endothelial cells and cells with the appearance of smooth muscle cells and lymphocytes. GroEL and bacteria were detected within intimal cells. Chlamydia pneumoniae, Porphyromonas gingivalis, Fusobacterium nucleatum, Tannerella forsythia, Prevotella intermedia, and Actinobacillus actinomycetemcomitans were found in 21%, 52%, 34%, 34%, 41%, and 17% of arteries, respectively. CONCLUSION: These results give evidence for a specific immune response associated with atherosclerosis. Whether bacteria initiate the observed inflammation in atherosclerotic lesions is not clear; however, the present study shows that maintenance of inflammation may be enhanced by the presence of periodontopathic bacteria.

Aggregatibacter actinomycetemcomitans↗

PubMed2006

Interleukin-1beta, interleukin-12 and interleukin-18 levels in gingival fluid and serum of patients with gingivitis and periodontitis.

INTRODUCTION: Cytokines are of major importance in periodontal disease progression. Interleukin-12 (IL-12) stimulates interferon-gamma production by T helper type 1 (Th1) cells while IL-18 induces Th1 responses when present with IL-12 but Th2 responses in the absence of IL-12. IL-1beta has been correlated with periodontal disease destruction. This study determined the local concentrations of these cytokines in sites of gingivitis and periodontitis. METHODS: Gingival crevicular fluid was collected from two sites in each of 10 gingivitis patients and from two gingivitis sites and two periodontitis sites from each of 10 periodontitis patients. Serum samples were also collected. IL-1beta, biologically active IL-12 p70, the IL-12 p40 subunit and IL-18 concentrations were determined by enzyme-linked immunoabsorbent assay. RESULTS: IL-1beta and IL-18 concentrations were higher in the gingival crevicular fluid from periodontitis patients than in that from gingivitis patients; IL-18 concentrations were higher than those of IL-1beta. Very little IL-12, either p40 or p70, was detected in the gingival crevicular fluid samples. In the serum, very low levels of cytokines were found. The level of serum IL-12 p40, however, was higher than in the fluid from periodontitis sites of periodontitis patients. CONCLUSION: The local production of IL-1beta and IL-18 in the gingival crevicular fluid increased with increasing inflammation and IL-18 was the predominant cytokine at both gingivitis and periodontitis sites. Very little IL-12 was detected with levels decreasing with increasing inflammation. These results suggest that there is an association between severity of periodontal disease and levels of IL-1, IL-12 and IL-18.

Adult↗

PubMed2006

The role of cyclic-AMP on arginase activity by a murine macrophage cell line (RAW264.7) stimulated with lipopolysaccharide from Actinobacillus actinomycetemcomitans.

AIMS: The aim of the present study was to determine the role of cyclic adenosine monophosphate (cAMP) on arginase activity in a murine macrophage cell line (RAW264.7 cells) stimulated with lipopolysaccharide (LPS) from Actinobacillus actinomycetemcomitans. MATERIALS AND METHODS: The cells were treated with A. actinomycetemcomitans LPS for 24 h. The effects of SQ22536 (an adenylyl cyclase inhibitor), ODQ (a guanylyl cyclase inhibitor), dibutyryl cAMP (a cAMP analog), 8-bromo cyclic guanosine monophosphate (a cGMP analog), forskolin (an adenylyl cylase activator), and cycloheximide (a protein synthesis inhibitor) on arginase activity in A. actinomycetemcomitans LPS-stimulated RAW264.7 cells were also determined. Arginase activity was assessed in LPS-stimulated cells in the presence of 3-isobutyl-1-methylxanthine (IBMX), siguazodan and rolipram [phosphodiesterase (PDE) inhibitors] as well as KT5720 [a protein kinase A (PKA) inhibitor]. RESULTS: Arginase activity in A. actinomycetemcomitans LPS-stimulated RAW264.7 cells was suppressed by SQ22536 but not ODQ. Enhancement of arginase activity was observed in the presence of cAMP analog or forskolin but not cGMP analog. Cycloheximide blocked arginase activity in the cells in the presence of cAMP analog or forskolin with or without A. actinomycetemcomitans LPS. IBMX augmented arginase activity in A. actinomycetemcomitans LPS-stimulated cells. Rolipram (a PDE4 inhibitor) increased the levels of arginase activity higher than siguazodan (a PDE3 inhibitor) in the antigen-stimulated cells. The effect of cAMP analog or forskolin on arginase activity in the presence or absence of A. actinomycetemcomitans LPS was blocked by the PKA inhibitor (KT5720). CONCLUSION: The results of the present study suggest that A. actinomycetemcomitans LPS may stimulate arginase activity in murine macrophages (RAW264.7 cells) in a cAMP-PKA-dependent pathway.

1-Methyl-3-isobutylxanthine↗

PubMed2006

The role of CD4+ and CD8+ T cells on antibody production by murine Peyer's patch cells following mucosal presentation of Actinomyces viscosus.

The aim of this study was to determine the role of CD4 and CD8 cells on specific antibody production by murine Peyer's patch (PP) cells after oral immunization with Actinomyces viscosus in mice. Female DBA/2 mice were orally immunized with three low doses of heat-killed A. viscosus. Sham-immunized mice served as a control group. Mice were depleted of CD4 or CD8 cells by intraperitoneal injection of anti-CD4 or anti-CD8 antibodies daily for 3 days before oral immunization. One week after the last oral immunization, PPs were removed and cell suspensions were cultured with A. viscosus. Specific antibody production in the culture supernatants was assessed by enzyme-linked immunosorbent assay. The results showed that oral immunization with A. viscosus induced a predominant specific immunoglobulin A (IgA) response by PP cells and, to a lesser extent, IgM antibodies. Depletion of CD4 but not CD8 cells suppressed the production of specific antibodies. These results suggest that oral immunization with low doses of A. viscosus may induce the production of specific antibodies by murine PP cells in a CD4-cell-dependent fashion.

Actinomyces viscosus↗

PubMed2006

The induction of oral tolerance to Actinomyces viscosus in mice.

OBJECTIVES: To determine whether oral tolerance with the oral bacterium Actinomyces viscosus was inducible in mice. MATERIALS AND METHODS: Mice were intragastrically (i.g.) and then intraperitoneally (i.p.) immunized with heat-killed A. viscosus. A control group of mice received only saline. A delayed type hypersensitivity (DTH) response and the levels of isotype specific antibodies were assessed. Spleen cells from mice that were i.g. immunized with A. viscosus were transferred to A. viscosus-primed mice in vivo and in vitro. Furthermore, mice were i.g. immunized with saline or A. viscosus and then challenged i.p. with saline, A. viscosus, or Porphyromonas gingivalis. RESULTS: Intragastric immunization with A. viscosus suppressed both DTH and serum specific antibodies to A. viscosus. DTH suppression lasted until week 4, while serum immunoglobulin (Ig)A and both IgG and IgM specific antibody levels remained suppressed up to week 8 and 12 respectively. IgG specific antibody suppression was transferable. The DTH response and serum antibodies specific to A. viscosus were suppressed in mice after i.g. challenged with A. viscosus but not P. gingivalis. CONCLUSION: Mucosal presentation of A. viscosus in mice led to the suppression of immune response to this bacterium in an antigen-specific fashion. Tolerance of DTH response was short lived, while suppression of antigen-specific IgG antibodies in mucosally tolerized mice was long-lasting.

Actinomyces viscosus↗

PubMed2005

Local application of prostaglandin E2 reduces trap, calcitonin receptor and metalloproteinase-2 immunoreactivity in the rat periodontium.

It has been shown that prostaglandin E2 (PGE2) locally released adjacent to the mandible over a 20-day period increases alveolar bone area, in part, due to a reduction in the percentage of eroded surface. To determine the effect of PGE2 on alveolar bone resorption, left mandibles from 24 Lewis rats were treated over a 20-day period with a local application of PGE2 (0.1, 0.05 or 0.025 mg/day) or placebo. The right side served as the non-treated matched control. Tissue sections were stained for tartrate resistant acid phosphatase (TRAP) calcitonin receptor (CTR) and metalloproteinase-2 (MMP-2). Matched samples were analysed by Wilcoxon matched pairs test and, a non-parametric one-way analysis of variance compared groups of treatment. Those tissues treated with PGE2 at doses of 0.1 and 0.05 mg/day showed significantly reduced numbers of TRAP and CTR-positive multinucleated cells compared with matched controls (p<0.005), as well as significantly reduced numbers of TRAP- and CTR-positive multinucleated cells when compared with the placebo-treated group (p<0.001). The number of periodontal ligament cells expressing MMP-2 was also significantly reduced in tissues treated with the two higher doses of PGE2 (p<0.001) comparing with both matched controls and the placebo-treated group. Following a 20-day period, locally released PGE2 at doses of 0.1 and 0.05 mg/day appears to affect alveolar bone resorption in the periodontium of rats, as the number of multinucleated cells expressing TRAP and CTR are significantly reduced. Furthermore, the same doses of PGE2 also significantly reduced the expression of MMP-2 by the periodontal cells.

Acid Phosphatase↗

PubMed2005

Immunohistological analysis of Tannerella forsythia-induced lesions in a murine model.

Tannerella forsythia has been implicated as a defined periodontal pathogen. In the present study a mouse model was used to determine the phenotype of leukocytes in the lesions induced by subcutaneous injections of either live (group A) or nonviable (group B) T. forsythia. Control mice (group C) received the vehicle only. Lesions were excised at days 1, 2, 4, and 7. An avidin-biotin immunoperoxidase method was used to stain infiltrating CD4+ and CD8+ T cells, CD14+ macrophages, CD19+ B cells, and neutrophils. Hematoxylin and eosin sections demonstrated lesions with central necrotic cores surrounded by neutrophils, macrophages and lymphocytes in both group A and group B mice. Lesions from control mice exhibited no or only occasional solitary leukocytes. In both groups A and B, neutrophils were the dominant leukocyte in the lesion 1 day after injection, the numbers decreasing over the 7-day experimental period. There was a relatively low mean percent of CD4+ and CD8+ T cells in the lesions and, whereas the percent of CD8+ T cells remained constant, there was a significant increase in the percent of CD4+ T cells at day 7. This increase was more evident in group A mice. The mean percent of CD14+ macrophages and CD19+ B cells remained low over the experimental period, although there was a significantly higher mean percent of CD19+ B cells at day 1. In conclusion, the results showed that immunization of mice with live T. forsythia induced a stronger immune response than nonviable organisms. The inflammatory response presented as a nonspecific immune response with evidence of an adaptive (T-cell) response by day 7. Unlike Porphyromonas gingivalis, there was no inhibition of neutrophil migration.

Abscess↗

PubMed2005

Cross-reactivity of GroEL antibodies with human heat shock protein 60 and quantification of pathogens in atherosclerosis.

BACKGROUND/AIMS: Chronic infections such as those caused by Chlamydia pneumoniae and periodontopathic bacteria such as Porphyromonas gingivalis have been associated with atherosclerosis, possibly due to cross-reactivity of the immune response to bacterial GroEL with human heat shock protein (hHSP) 60. METHODS: We examined the cross-reactivity of anti-GroEL and anti-P. gingivalis antibodies with hHSP60 in atherosclerosis patients and quantified a panel of six pathogens in atheromas. RESULTS: After absorption of plasma samples with hHSP60, there were variable reductions in the levels of anti-GroEL and anti-P. gingivalis antibodies, suggesting that these antibodies cross-reacted with hHSP60. All of the artery specimens were positive for P. gingivalis. Fusobacterium nucleatum, Tannerella forsythia, C. pneumoniae, Helicobacter pylori, and Haemophilus influenzae were found in 84%, 48%, 28%, 4%, and 4% of arteries, respectively. The prevalence of the three periodontopathic microorganisms, P. gingivalis, F. nucleatum and T. forsythia, was significantly higher than that of the remaining three microorganisms. CONCLUSIONS: These results support the hypothesis that in some patients, cross-reactivity of the immune response to bacterial HSPs including those of periodontal pathogens, with arterial endothelial cells expressing hHSP60 may be a possible mechanism for the association between atherosclerosis and periodontal infection.

Aged↗

PubMed2005

The distribution of Tannerella forsythia in an adolescent and adult population.

BACKGROUND: The fact that Tannerella forsythia, an important periopathogen, is difficult to cultivate from mixed infections has impeded precise estimates of its distribution within a given population. In order to discern T. forsythia alone from the mixed infection of plaque, the use of sensitive 16S ribosomal RNA based polymerase chain reaction (PCR) detection is necessary. OBJECTIVES: The aim of the present study was to determine the distribution of T. forsythia in an adult and in an adolescent population. MATERIAL AND METHODS: Subgingival plaque samples were obtained from 498 Australian adults and from 228 adolescent subjects from Manchester, UK. Tannerella forsythia was detected using PCR and confirmed by restriction analysis. Semi-quantitation of the organisms was carried out using two specific primers of differing sensitivities. RESULTS: In the adolescent population, 25% were found to carry T. forsythia, albeit in relatively low numbers. In the adult population, a total of 37.8% and 11% were found to carry the organism with primer 2 and primer 1, respectively, suggesting that around 27% had between 10(3) and 10(7) organisms. Although there was an apparent increased proportion of T. forsythia positive subjects in those aged > or = 50 years, this was not statistical significant. However, T. forsythia positive male smokers showed increased disease severity compared with T. forsythia negative subjects. CONCLUSION: This study has shown that at least 25% of the adolescent population carry low numbers of T. forsythia, whereas at least 37% of adults carry the organism, with some 11% having relatively high numbers. The relationship between T. forsythia and disease progression in these populations, however, remains to be determined.

Adolescent↗

PubMed2005

Regulatory T-cells infiltrate periodontal disease tissues.

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.

Aged↗

PubMed2004

Prostaglandin E2 enhances alveolar bone formation in the rat mandible.

Prostaglandin E2 (PGE2) induces bone formation in stress-bearing bones. The mandible, a stress-bearing bone, is loaded daily during mastication. The aim of this study was to determine if PGE2 delivered locally to the mandible over 20 days enhances alveolar bone deposition. In 18 Lewis rats, controlled-release pellets containing PGE2 were implanted on the buccal aspect on the left-hand side of the mandible, mesial to the root of the first molar. Controlled-release pellets locally delivered 0.1, 0.05, or 0.025 mg/day of PGE2. The right side of the mandible was used as a matched control for each animal. Six sham-treated animals were implanted with a placebo pellet. On days 7 and 19, animals were injected with the bone markers tetracycline and calcein, respectively. On day 21, animals were sacrificed and undecalcified tissues obtained for morphometrical analysis. Morphometrical measurements were analyzed by paired t test to determine differences between the matched samples and one-way ANOVA to compare the different treatment groups. A significant increase in alveolar bone area was observed in mandibles treated with 0.1 and 0.05 mg/day when compared with matched controls and the placebo group. This was accompanied by a significant increase in alveolar bone height and width. The proportions of double-labeled surface (dLS), the mineral apposition rate (MAR), and bone formation rate (BFR) were significantly increased in mandibles treated with the two higher doses of PGE2. The proportion of resorptive surface (RS) was significantly reduced in these two groups. It is concluded that PGE2 induces alveolar bone formation in the mandible when locally delivered at a dose of 0.1 or 0.05 mg/day for 20 days.

Animals↗

PubMed2004

L-arginine-dependent nitric oxide production of a murine macrophage-like RAW 264.7 cell line stimulated with Porphyromonas gingivalis lipopolysaccharide.

The aim of this study was to determine nitric oxide (NO) production of a murine macrophage cell line (RAW 264.7 cells) when stimulated with Porphyromonas gingivalis lipopolysaccharides (Pg-LPS). RAW 264.7 cells were incubated with i) various concentrations of Pg-LPS or Salmonella typhosa LPS (St-LPS), ii) Pg-LPS with or without L-arginine and/or NG-monomethyl-L-arginine (NMMA), an arginine analog or iii) Pg-LPS and interferon-gamma (IFN-gamma) with or without anti-IFN-gamma antibodies or interleukin-10 (IL-10). Tissue culture supernatants were assayed for NO levels after 24 h in culture. NO was not observed in tissue culture supernatants of RAW 264.7 cells following stimulation with Pg-LPS, but was observed after stimulation with St-LPS. Exogenous L-arginine restored the ability of Pg-LPS to induce NO production; however, the increase in NO levels of cells stimulated with Pg-LPS with exogenous L-arginine was abolished by NMMA. IFN-gamma induced independent NO production by Pg-LPS-stimulated macrophages and this stimulatory effect of IFN-gamma could be completely suppressed by anti-IFN-gamma antibodies and IL-10. These results suggest that Pg-LPS is able to stimulate NO production in the RAW 264.7 macrophage cell model in an L-arginine-dependent mechanism which is itself independent of the action of IFN-gamma.

Analysis of Variance↗

PubMed2004

T-cell clonality to Porphyromonas gingivalis and human heat shock protein 60s in patients with atherosclerosis and periodontitis.

Individuals with periodontitis have been reported to have a significantly increased risk of developing coronary heart disease. Several studies have demonstrated that the immune response to heat shock protein 60 (HSP60) may be involved in the pathogenesis of both atherosclerosis and chronic periodontitis. To investigate this possible link between these diseases, cellular and humoral immune responses to HSP60 in atherosclerosis patients were compared with those in periodontitis patients and healthy subjects using human and Porphyromonas gingivalis HSP60 (GroEL) as antigens. Antibody levels to both human and P. gingivalis HSP60s were the highest in atherosclerosis patients, followed by periodontitis patients and healthy subjects. Clonal analysis of the T cells clearly demonstrated the presence of not only human HSP60- but also P. gingivalis GroEL-reactive T-cell populations in the peripheral circulation of atherosclerosis patients. Furthermore, these HSP60-reactive T cells seemed to be present in atherosclerotic lesions in some patients. These results suggest that T-cell clones with the same specificity may be involved in the pathogenesis of the different diseases.

Adult↗

PubMed2004

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

We have shown previously that both humoral and cellular immune responses to heat shock protein 60 (HSP60) are elevated in chronic periodontitis patients compared with non-diseased subjects. The aim of the present study was to determine whether periodontal treatment could influence the level of serum antibodies to human HSP60 and Porphyromonas gingivalis GroEL, a bacterial homologue of human HSP60. Sera were obtained from 21 patients with moderate to advanced chronic periodontitis at the baseline examination and again after completion of treatment. Antibody levels were determined using an enzyme-linked immunosorbent assay. The mean anti-P. gingivalis GroEL antibody levels were down-regulated significantly by periodontal treatment when recombinant P. gingivalis GroEL was used as an antigen, whereas antibody levels to P. gingivalis GroEL-specific peptide were significantly elevated following successful periodontal therapy. The mean level of anti-human HSP60 antibody remained unchanged although individual levels of antibody either increased or decreased after periodontal treatment, suggesting that synthesis of these antibodies might be regulated independently during the course of periodontal infection. Although their regulatory mechanisms in chronic infection are not understood, further study would provide insight not only into the role of these antibodies in the pathogenesis of periodontitis but also into the possible link between periodontitis and systemic diseases such as coronary heart disease.

Adult↗