4.2 Article

Porphyromonas gingivalis Lipopolysaccharide-Induced B Cell Differ-entiation by Toll-like Receptors 2 and 4

Journal

PROTEIN AND PEPTIDE LETTERS
Volume 29, Issue 1, Pages 46-56

Publisher

BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/0929866528666211118085828

Keywords

P; gingivalis; lipopolysaccharide; interleukin-10; toll-like receptor; Breg cell; periodontitis

Funding

  1. National Nature Science Foundation of China [81470740]

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This study found that P. gingivalis stimulates B cells to produce IL-10 via TLR2/4, and the CD5+ B1 subset is the main source of IL-10+ Breg cells. Under P. gingivalis LPS stimulation, CD5+ IgM+ CD93-IL-10+ B cell subset increases significantly.
Background: Porphyromonas gingivalis (P. gingivalis) is a pathogenic bacterium widely present in subgingival plaques of patients with periodontitis. It induces periodontitis with bone loss as its main feature by changing the number and composition of symbiotic microorganisms, as well as inducing the natural immune response of the host. However, the mechanism of the latter remains unclear. Objective: This study aims to investigate the effect ofP. gingivalis lipopolysaccharide (LPS) on regulatory B cells (Breg) in the occurrence and development of periodontitis. Methods: We detected the mRNA levels of IL-10 in B cells under the stimulation of P. gingivalis LPS and/or E. coli LPS, distinguished IL-10-producing cells from different B cell subgroups using flow cytometry. Through toll-like receptor (TLR) knockout mice, the role of TLR2 and TLR4 in this process was also evaluated. Results: Results showed thatP. gingivalis stimulated B cells to produce IL-10 via TLR2/4. CD5+B1 subset is the main source of IL-10+Breg cell. UnderP. gingivalis LPS stimulation, CD5+IgM+CD93-IL-10+B cell subset increased significantly, which was regulated through TL R2/4. Conclusion: The results of this study provides new insights into the immunopathogenic mechanism of P. gingivalis , preliminarily discussed the effect of P. gingivalis on the production of Breg, and present a theoretical foundation for subsequent investigations on the occurrence and development of periodontitis.

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