Changes in Expression of the Membrane Receptors CD14, MHC-II, SR-A, and TLR4 in Tissue-Specific Monocytes/Macrophages Following Porphyromonas gingivalis–LPS Stimulation

The aim of the study was to provide a theoretical foundation for understanding the relationship between periodontal diseases and systemic diseases by examining the inflammatory effect of Porphyromonas gingivalis lipopolysaccharide (LPS) on monocytes/macrophages isolated from tissues distinct from the oral cavity in normal and hyperlipidemic New Zealand white rabbits. Macrophages were isolated from four separate tissues (mononuclear cells from blood, alveolar macrophages, peritoneal macrophages, and Kupffer cells) from both normal and hyperlipidemic New Zealand white rabbits. Cells were either stimulated for 24 h in vitro with P. gingivalis–LPS or Escherichia coli–LPS, or were pre-treated with IL-10 before P. gingivalis–LPS treatment. RNA was isolated and the expression of SR-A, TLR4, CD14, and MHC-II measured by RT-PCR. For MHC-II, the suppression effects of P. gingivalis–LPS were similar to the effects of E. coli–LPS in all macrophages examined. In general, the magnitude of the effects of P. gingivalis–LPS on gene expression was lower than that of E. coli–LPS, and there were differences in the relative membrane receptors between the two, implying that the two LPSs stimulate different responses. IL-10 increased the expression of the defensive receptor SR-A and decreased the expression of CD14, TLR4, and the antigen-presenting molecule MHC-II in all types of macrophages examined, regardless of hyperlipidemic state. These data are consistent with an anti-inflammatory effect of IL-10. P. gingivalis–LPS is an activator of gene expression in macrophages isolated from tissues distinct from the oral cavity.