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B cells promote obesity-associated periodontitis and oral pathogen-associated inflammation.

ABSTRACT: Individuals with T2D and PD suffer significantly from the ability of one disease to intensify the other. Disease-associated inflammation is one mechanism thought to fuel this pathogenic feed-forward loop. Several lines of evidence indicate that proinflammatory B cells promote T2D and PD; thus, B cells are top candidates for a cell type that predisposes PD in T2D. To test directly the role of B cells in T2D-associated PD, we compared outcomes from oral Porphyromonas gingivalis challenge of lean WT or B cell-null mice with outcomes from mice that were obese and insulin-resistant before challenge. Obese WT mice responded to oral P. gingivalis challenge with significant periodontal bone loss, whereas obese B cell-null mice were protected completely from PD. By contrast, lean WT and B cell-null mice suffer similar periodontal bone loss in response to oral pathogen. B cells from obese/insulin-resistant hosts also support oral osteoclastogenesis and both oral and systemic production of inflammatory cytokines, including pro-osteoclastogenic TNF-? and MIP-2, an ortholog of human IL-8. B cells furthermore impact AT inflammation in obese, P. gingivalis-infected hosts. Taken together, these data show that fundamentally different mechanisms regulate PD in lean and obese hosts, with B cells able to promote PD only if the hosts are "primed" by obesity. These results justify more intense analysis of obesity-associated changes in B cells that predispose PD in human T2D.

SUBMITTER: Zhu M

PROVIDER: S-EPMC4101090 | biostudies-other | 2014 Aug

REPOSITORIES: biostudies-other

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B cells promote obesity-associated periodontitis and oral pathogen-associated inflammation.

Zhu Min M Belkina Anna C AC DeFuria Jason J Carr Jordan D JD Van Dyke Thomas E TE Gyurko Robert R Nikolajczyk Barbara S BS

Journal of leukocyte biology 20140429 2

Individuals with T2D and PD suffer significantly from the ability of one disease to intensify the other. Disease-associated inflammation is one mechanism thought to fuel this pathogenic feed-forward loop. Several lines of evidence indicate that proinflammatory B cells promote T2D and PD; thus, B cells are top candidates for a cell type that predisposes PD in T2D. To test directly the role of B cells in T2D-associated PD, we compared outcomes from oral Porphyromonas gingivalis challenge of lean W ...[more]

PMID: 24782490

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Project description:BACKGROUND:Non-surgical periodontal therapy (NSPT) known as gold standard treatment in managing periodontitis. The aim of this study was to investigate the response of NSPT in periodontitis subjects who were obese. Clinical parameters of periodontitis, changes in serum resistin and periodontal pathogens in subgingival plaque were compared before and after NSPT in periodontitis subjects who were obese and with normal weight. METHODS:A total of 48 periodontitis subjects (obese, n = 18; normal weight, n = 30) were recruited (hereafter will be referred as participants) to participate into a prospective, before and after clinical trial. Obesity status is defined by body mass index (BMI) criteria (obese: ≥30 kg/ m2; normal weight < 25 kg/m2). Visible Plaque Index (VPI), Gingival Bleeding Index (GBI), Probing Pocket Depth (PPD) and Clinical Attachment Loss (CAL) were recorded; and serum and plaque were collected at baseline and following 12 weeks post-NSPT. Serum resistin level was analyzed using enzyme-linked immune-sorbant assay (ELISA), while detection of periodontal pathogens in dental plaque were carried out using real time PCR (qPCR). RESULTS:Following NSPT, means VPI and GBI showed significant improvement between obese and normal weight groups (p < 0.05), but no difference in means PPD and CAL was observed between groups. Obesity remained as a predictor for VPI and GBI after adjusting for smoking habit. No significant difference was observed in serum resistin level and mean counts for P. gingivalis, T. forsythia, and P. intermedia between obese and normal weight groups following NSPT. CONCLUSIONS:Regardless of obesity status, NSPT has a significant impact on VPI and GBI in periodontitis subjects. However, the impact of NSPT towards serum resistin and periodontal pathogens was non-significant in those with periodontitis. TRIAL REGISTRATION:This study followed the Consolidation Standards of Reporting Trials Statement and retrospectively registered on 26/11/2015 at clinicaltrials.gov (No. NCT02618486).

Dataset Information

B cells promote obesity-associated periodontitis and oral pathogen-associated inflammation.

Publications

B cells promote obesity-associated periodontitis and oral pathogen-associated inflammation.

Similar Datasets

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