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Published on: May 15, 2019
Lipoteichoic acid partially contributes to the inflammatory responses to Enterococcus faecalis
Jung Eun Baik1, Young Hee Ryu, Ji Young Han
1Department of Oral Microbiology & Immunology, Dental Research Institute and BK21 Program, School of Dentistry, Seoul National University, Seoul, Republic of Korea.
Lipoteichoic acid (LTA) from Enterococcus faecalis, a key pathogen in apical periodontitis, significantly activates macrophages. This bacterial component stimulates inflammatory responses by engaging Toll-like receptor 2 (TLR2) and nuclear factor-kappa B (NF-kappaB).
Area of Science:
- Immunology
- Microbiology
- Oral Biology
Background:
- Enterococcus faecalis is a significant pathogen associated with refractory apical periodontitis.
- Lipoteichoic acid (LTA) is recognized as a major virulence factor in gram-positive bacteria.
- Understanding bacterial components' roles in host immune response is crucial for treating infections.
Purpose of the Study:
- To investigate the immunomodulatory effects of highly pure Enterococcus faecalis lipoteichoic acid (LTA).
- To compare the macrophage-stimulating ability of E. faecalis LTA with killed whole bacterial cells.
- To elucidate the specific Toll-like receptors (TLRs) and signaling pathways involved in LTA-induced immune responses.
Main Methods:
- Preparation of highly pure lipoteichoic acid (LTA) from Enterococcus faecalis.
- Exposure of RAW 264.7 murine macrophage cell line to varying concentrations of E. faecalis LTA and killed whole cells.
- Measurement of inflammatory mediators: tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO).
- Assessment of Toll-like receptor (TLR) activation (TLR2 and TLR4).
- Analysis of nuclear factor-kappa B (NF-kappaB) DNA-binding activity.
Main Results:
- E. faecalis LTA significantly induced concentration-dependent production of TNF-alpha and NO in RAW 264.7 cells.
- LTA specifically stimulated Toll-like receptor 2 (TLR2) but not TLR4.
- LTA enhanced the DNA-binding activity of nuclear factor-kappa B (NF-kappaB), a key transcription factor in inflammation.
- Heat-killed E. faecalis stimulated both TLR2 and TLR4, inducing significant TNF-alpha and NO levels.
Conclusions:
- Lipoteichoic acid (LTA) from Enterococcus faecalis is a potent stimulator of macrophage inflammatory responses.
- LTA contributes partially to the inflammatory effects induced by E. faecalis through TLR2 and NF-kappaB activation.
- These findings highlight LTA as a critical virulence factor in E. faecalis-associated infections like apical periodontitis.
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