Serum Antibodies to Porphyromonas gingivalis Chaperone HtpG Predict Health in Periodontitis Susceptible Patients

Department of Biologic and Materials Sciences, The University of Michigan School of Dentistry, Ann Arbor, Michigan, United States of America.
PLoS ONE (Impact Factor: 3.23). 02/2008; 3(4):e1984. DOI: 10.1371/journal.pone.0001984
Source: PubMed


Chaperones are ubiquitous conserved proteins critical in stabilization of new proteins, repair/removal of defective proteins and immunodominant antigens in innate and adaptive immunity. Periodontal disease is a chronic inflammatory infection associated with infection by Porphyromonas gingivalis that culminates in the destruction of the supporting structures of the teeth. We previously reported studies of serum antibodies reactive with the human chaperone Hsp90 in gingivitis, a reversible form of gingival disease confined to the oral soft tissues. In those studies, antibodies were at their highest levels in subjects with the best oral health. We hypothesized that antibodies to the HSP90 homologue of P. gingivalis (HtpG) might be associated with protection/resistance against destructive periodontitis.

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    • "These include lipopolysaccharide (Bainbridge et al., 1997) and a 40-kDa outer membrane antigen (Momoi et al., 2008). Antibody responses to 43-kDa fimbrial protein, Pga30 (30-kDa antigenic protein), PrtC (38-kDa collagenase), and HtpG (heat-shock protein 90 homologue) have also been reported (Condorelli et al., 1998; Hendtlass et al., 2000; Beikler et al., 2003; Shelburne et al., 2008). It is therefore plausible that antibodies to these proteins are involved in case 14. "
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    ABSTRACT: Porphyromonas gingivalis is a keystone periodontal pathogen. Histologocally, the gingival tissue in periodontitis shows dense infiltration of plasma cells. However, antigens recognized by antibodies secreted from the immunocytes remain unknown. The enzyme-labeled antigen method was applied to detecting plasma cells producing P. gingivalis-specific antibodies in biopsied gingival tissue of periodontitis. N-terminally biotinylated P. gingivalis antigens, Ag53 and four gingipain domains (Arg-pro, Arg-hgp, Lys-pro and Lys-hgp) were prepared by the cell-free protein synthesis system using the wheat germ extract. With these five labeled proteins as probes, 20 lesions of periodontitis were evaluated. With the AlphaScreen method, the antibodies against any one of the five P. gingivalis antigens were detected in 11 (55%) samples of sera, and 17 (85%) of tissue extracts. With the enzyme-labeled antigen method on paraformaldehyde-fixed frozen sections of gingival tissue, plasma cells were labeled with any one of the five antigens in 17 (94%) of 18 specimens, in which evaluable plasma cells were detected. The positivity rates in periodontitis were significantly higher than those in radicular cyst we have reported (20% in sera and 33% in tissue extracts with the AlphaScreen method, and 25% with the enzyme-labeled antigen method, Tsuge et al., J Histochem Cytochem, 2011). Our findings directly indicate that antibodies reactive to P. gingivalis are locally produced in the gingival lesions, and that inflammatory reactions against P. gingivalis are involved in periodontitis. This article is protected by copyright. All rights reserved.
    Full-text · Article · Apr 2014
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    • "Subgingival plaque biofilm was collected from the mesiobuccal aspect of all teeth at baseline, 6, and 12 mos as described previously (Shelburne et al., 2008). The detection of Porphyromonas gingivalis , Prevotella intermedia, Tannerella forsythia, Fusobacterium nucleatum, Treponema denticola, and Campylobacter rectus was quantified by qPCR as described previously (Mullally et al., 2000). "
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    ABSTRACT: The purpose of this study was to determine the role of saliva-derived biomarkers and periodontal pathogens during periodontal disease progression (PDP). One hundred human participants were recruited into a 12-month investigation. They were seen bi-monthly for saliva and clinical measures and bi-annually for subtraction radiography, serum and plaque biofilm assessments. Saliva and serum were analyzed with protein arrays for 14 pro-inflammatory and bone turnover markers, while qPCR was used for detection of biofilm. A hierarchical clustering algorithm was used to group study participants based on clinical, microbiological, salivary/serum biomarkers, and PDP. Eighty-three individuals completed the six-month monitoring phase, with 39 [corrected] exhibiting PDP, while 44 [corrected] demonstrated stability. Participants assembled into three clusters based on periodontal pathogens, serum and salivary biomarkers. Cluster 1 members displayed high salivary biomarkers and biofilm; 71% [corrected] of these individuals were undergoing PDP. Cluster 2 members displayed low biofilm and biomarker levels; 76% [corrected] of these individuals were stable. Cluster 3 members were not discriminated by PDP status; however, cluster stratification followed groups 1 and 2 based on thresholds of salivary biomarkers and biofilm pathogens. The association of cluster membership to PDP was highly significant (p < 0.0007). [corrected] The use of salivary and biofilm biomarkers offers potential for the identification of PDP or stability ( number, CT00277745).
    Full-text · Article · Mar 2011 · Journal of dental research
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    • "Indeed, the classic periodontopathogens present a series of virulence factors that interfere with the protective responses of phagocytes (Venketaraman et al., 2008; Wang and Hajishengallis, 2008). Besides cellular immunity mechanisms, the humoral immunity axis involving Th2 and B-cells is also thought to contribute to host protection against periodontal pathogens (Shelburne et al., 2008). Also, antibodies produced in response to periodontal infection increase periodontopathogen phagocytosis by opsonization , and consequently enhance the phagocytes' bactericidal activities (Guentsch et al., 2009). "
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    ABSTRACT: Periodontal diseases (PD) are chronic infectious inflammatory diseases characterized by the destruction of tooth-supporting structures, being the presence of periodontopathogens required, but not sufficient, for disease development. As a general rule, host inflammatory mediators have been associated with tissue destruction, while anti-inflammatory mediators counteract and attenuate disease progression. With the discovery of several T-cell subsets bearing distinct immunoregulatory properties, this pro- vs. anti-inflammatory scenario became more complex, and a series of studies has hypothesized protective or destructive roles for Th1, Th2, Th17, and Treg subpopulations of polarized lymphocytes. Interestingly, the "protective vs. destructive" archetype is usually considered in a framework related to tissue destruction and disease progression. However, it is important to remember that periodontal diseases are infectious inflammatory conditions, and recent studies have demonstrated that cytokines (TNF-α and IFN-γ) considered harmful in the context of tissue destruction play important roles in the control of periodontal infection. Therefore, in this review, the state-of-the-art knowledge concerning the protective and destructive roles of host inflammatory immune response will be critically evaluated and discussed from the tissue destruction and control-of-infection viewpoints.
    Full-text · Article · Dec 2010 · Journal of dental research
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