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Periodontitis in the absence of B cells and specific anti‐bacterial antibody
Author(s) -
OliverBell J.,
Butcher J.P.,
Malcolm J.,
MacLeod M.K.L.,
Adrados Planell A.,
Campbell L.,
Nibbs R.J.B.,
Garside P.,
McInnes I.B.,
Culshaw S.
Publication year - 2015
Publication title -
molecular oral microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.18
H-Index - 77
eISSN - 2041-1014
pISSN - 2041-1006
DOI - 10.1111/omi.12082
Subject(s) - porphyromonas gingivalis , antibody , immune system , immunology , periodontitis , biology , b cell , rankl , cxcr5 , microbiology and biotechnology , germinal center , flow cytometry , receptor , medicine , activator (genetics)
Summary Periodontitis (PD) results from complex interactions between a dysbiotic oral microbiota and a dysregulated host immune response. The inflammatory infiltrate in the gingiva of PD patients includes an abundance of B cells, implicating these cells in the immunopathology. We sought to investigate the role of B cells in PD using a murine model. Wild‐type or B‐cell‐deficient (μMT) mice were orally infected with Porphyromonas gingivalis . One or six weeks following infection, lymphocyte populations in the gingiva and cervical draining lymph nodes ( dLN ) were analysed by flow cytometry; serum anti‐ P. gingivalis IgG antibody titers were measured by enzyme‐linked immunosorbent assay, and alveolar bone loss was determined. In wild‐type mice, the percentage of gingival B cells expressing receptor activator of nuclear factor‐κB ligand (RANKL) was significantly increased 1 week post‐infection (5.36% control versus 11% PD, P < 0.01). The percentage of Fas + GL7 + germinal centre B cells in the dLN was significantly increased at both 1 week (2.03% control versus 6.90% PD, P < 0.01) and 6 weeks (4.45% control versus 8.77% PD, P < 0.05) post‐infection. B‐cell‐deficient mice were protected from P. gingivalis ‐induced alveolar bone loss, with a lack of B‐cell proliferation and lack of CD4 + CD44 + CD62L − T‐cell generation in the dLN , and absence of serum anti‐ P. gingivalis antibodies. Our data imply a pathological role for B cells in PD, and that selective targeting of this immune axis may have a role in treating severe periodontal disease.