ArticleOral microbiology and immunology2009
Expression of receptor activator of nuclear factor-kappaB ligand by B cells in response to oral bacteria.
Article in Oral microbiology and immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 49 citations in OpenAlex.
- Evaluation of chemerin, fetuin-A, interleukin-34, and interleukin-13 levels following periodontal treatment in diabetes mellitus.Clinical oral investigations · 2025Trial
- Periodontal Inflamed Surface Area (PISA) associates with composites of salivary cytokines.PloS one · 2023Article
- Could AMPs and B-cells be the missing link in understanding periodontitis?Frontiers in immunology · 2022Article
- Differential involvement of the canonical and noncanonical inflammasomes in the immune response against infection by the periodontal bacteriaCurrent research in microbial sciences · 2021Article
- Persistent Abnormal Immunocytes Induced Systemic Bone Loss in Locally Irradiated Rats.Calcified tissue international · 2021Article
- B-Cell RANKL Contributes to Pathogen-Induced Alveolar Bone Loss in an Experimental Periodontitis Mouse Model.Frontiers in physiology · 2021Article
- Dysregulated systemic lymphocytes affect the balance of osteogenic/adipogenic differentiation of bone mesenchymal stem cells after local irradiation.Stem cell research & therapy · 2017Article
- Current Controversies on the Pathogenesis of Medication-Related Osteonecrosis of the Jaw.Dentistry journal · 2016Review
- Bone-immune cell crosstalk: bone diseases.Journal of immunology research · 2015Review
- Capsaicin inhibits Porphyromonas gingivalis growth, biofilm formation, gingivomucosal inflammatory cytokine secretion, and in vitro osteoclastogenesis.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2014Article
- RANKL expression in periodontal disease: where does RANKL come from?BioMed research international · 2014Review
- Periodontal disease immunology: 'double indemnity' in protecting the host.Periodontology 2000 · 2013Review
- Periodontal disease: linking the primary inflammation to bone loss.Clinical & developmental immunology · 2013Review
- RANKL cytokine: from pioneer of the osteoimmunology era to cure for a rare disease.Clinical & developmental immunology · 2013Review
- The role of the immune system in the physiopathology of osteoporosis.Clinical cases in mineral and bone metabolism : the official journal of the Italian Society of Osteoporosis, Mineral Metabolism, and Skeletal Diseases · 2012Article
- Epidemiology and pathogenesis of osteonecrosis of the jaw.Nature reviews. Rheumatology · 2011Review
- Selective serotonin reuptake inhibitors attenuate the antigen presentation from dendritic cells to effector T lymphocytes.FEMS immunology and medical microbiology · 2011Article
- TLR2 signaling and Th2 responses drive Tannerella forsythia-induced periodontal bone loss.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Interactions between the immune system and bone.World journal of orthopedics · 2011Article
- Cell-cell interactions in rheumatoid arthritis synovium.Rheumatic diseases clinics of North America · 2010Review
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Authors and funding
6 authors.
Funding
Abstract
introductionWe investigated receptor activator of nuclear factor-kappaB ligand (RANKL) expression by B lymphocytes during early and late aspects of the immune response to Aggregatibacter actinomycetemcomitans, a gram-negative, anaerobic bacterium associated with aggressive periodontal disease.
methodsExpression of messenger RNA transcripts (tumor necrosis factor-alpha, Toll-like receptors 4 and 9, interleukins 4 and 10, and RANKL) involved in early (1-day) and late (10-day) responses in cultured rat splenocytes was examined by reverse transcription-polymerase chain reaction (RT-PCR). The immune cell distribution (T, B, and natural killer cells and macrophages) in cultured rat splenocytes and RANKL expression in B cells were determined by flow cytometric analyses. B-cell capacity for induction of osteoclast differentiation was evaluated by coculture with RAW 264.7 cells followed by a tartrate-resistant acid phosphatase (TRAP) activity assay.
resultsThe expression levels of interleukins 4 and 10 in cultured cells were not changed in the presence of A. actinomycetemcomitans until cultured for 3 days, and peaked after 7 days. After culture for 10 days, the percentages of B and T cells, the overall RANKL messenger RNA transcripts, and the percentage of RANKL-expressing immunoglobulin G-positive cells were significantly increased in the presence of A. actinomycetemcomitans. These increases were considerably greater in cells isolated from A. actinomycetemcomitans-immunized animals than from non-immunized animals. RAW 264.7 cells demonstrated significantly increased TRAP activity when cocultured with B cells from A. actinomycetemcomitans-immunized animals. The addition of human osteoprotegerin-Fc to the culture significantly diminished such increases.
conclusionThis study suggests that B-lymphocyte involvement in the immune response to A. actinomycetemcomitans through upregulation of RANKL expression potentially contribute to bone resorption in periodontal disease.
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