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 of P. 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 that P. gingivalis stimulated B cells to produce IL-10 via TLR2/4. CD5+B1 subset is the main source of IL-10+Breg cell. Under P. gingivalis LPS stimulation, CD5+IgM+CD93-IL-10+B cell subset increased significantly, which was regulated through TLR2/ 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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