B cells from periodontal disease patients express surface Toll-like receptor 4

Hyunjin Shin, Yue Zhang, Madhumita Jagannathan, Hatice Hasturk, Alpdogan Kantarci, Hongsheng Liu, Thomas E. Van Dyke, Lisa M. Ganley-Leal, Barbara S. Nikolajczyk

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


Chronic systemic inflammation links periodontal disease (PD) to increased incidence of cardiovascular disease. Activation of TLRs, particularly TLR4, promotes chronic inflammation in PD by stimulating myeloid cells. B cells from healthy individuals are generally refractory to TLR4 agonists as a result of low surface TLR4 expression. Unexpectedly, a significantly increased percentage of gingival and peripheral blood B cells from patients with PD expressed surface TLR4. Surface expression correlated with an active TLR4 promoter that mimicked the TLR4 promoter in neutrophils. B cells from PD patients were surface myeloid differentiation protein 2-positive and also packaged the enhancer of a proinflammatory cytokine, IL-1β, into an active structure, demonstrating that these cells harbor key characteristics of proinflammatory cell types. Furthermore, B cells lacked activating signatures of a natural IL-1β inhibitor, IL-1 receptor antagonist. Surprisingly, despite multiple signatures of proinflammatory cells, freshly isolated B cells from PD patients had decreased expression of TLR pathway genes compared with B cells from healthy individuals. Decreases in inflammatory gene expression were even more dramatic in B cells stimulated with a TLR4 ligand from a periodontal pathogen, Porphyromonas gingivalis LPS 1690. In contrast, B cell TLR4 was not activated by the prototypic TLR4 ligand Escherichia coli LPS. These findings raise the unexpected possibility that TLR4 engagement modulates B cell activation in PD patients.

Original languageEnglish
Pages (from-to)648-655
Number of pages8
JournalJournal of Leukocyte Biology
Issue number4
StatePublished - Apr 1 2009


  • Bacterial infection
  • Gene regulation
  • Human
  • Inflammation
  • Molecular biology

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Cell Biology


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