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Changes in Expression of the Membrane Receptors CD14, MHC-II, SR-A, and TLR4 in Tissue-Specific Monocytes/Macrophages
Chunfang Wu1, Chongwu Liu2, Kai Luo1
1Affiliated Stomatological Hospital of Fujian Medical University, 246 Yangqiao Zhong Road, Fuzhou, Fujian Province, 35002, China.
Abstract:
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.
Insights
Porphyromonas gingivalis lipopolysaccharide (LPS) activates gene expression in macrophages outside the mouth, suggesting a link between periodontal disease and systemic inflammation. Interleukin-10 (IL-10) exhibits anti-inflammatory effects by modulating macrophage responses.
Area of Science:
- Immunology
- Periodontology
- Systemic Inflammation
Background:
- Periodontal diseases are linked to systemic conditions.
- Porphyromonas gingivalis lipopolysaccharide (LPS) is a key factor in periodontal disease.
- Understanding LPS effects on extra-oral macrophages is crucial for systemic disease research.
Purpose of the Study:
- To investigate the inflammatory effects of Porphyromonas gingivalis LPS on macrophages from various tissues.
- To compare the effects of P. gingivalis LPS with Escherichia coli LPS.
- To examine the role of Interleukin-10 (IL-10) in modulating these inflammatory responses.
Main Methods:
- Macrophages were isolated from normal and hyperlipidemic rabbits (blood, alveolar, peritoneal, Kupffer cells).
- Cells were stimulated with P. gingivalis LPS or E. coli LPS, with or without IL-10 pre-treatment.
- Gene expression of SR-A, TLR4, CD14, and MHC-II was analyzed using RT-PCR.
Main Results:
- P. gingivalis LPS activated gene expression in macrophages from tissues distinct from the oral cavity.
- The magnitude of P. gingivalis LPS effects was generally lower than E. coli LPS, indicating different responses.
- IL-10 demonstrated anti-inflammatory effects, upregulating SR-A and downregulating CD14, TLR4, and MHC-II.
Conclusions:
- P. gingivalis LPS can activate gene expression in macrophages beyond the oral cavity.
- Distinct LPS types elicit different macrophage responses.
- IL-10 exhibits significant anti-inflammatory properties in modulating macrophage inflammatory pathways.
