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Enterococcus faecalis Demonstrates Pathogenicity through Increased Attachment in an Ex Vivo Polymicrobial Pulpal
Wayne Nishio Ayre1, Genevieve Melling2, Camille Cuveillier2
1School of Dentistry, Cardiff University, Cardiff, United Kingdom ayrewn@cardiff.ac.uk.
Infection and Immunity
|February 28, 2018
Summary
Enterococcus faecalis drives inflammation in polymicrobial dental infections by strongly attaching to pulpal vasculature. This bacterial adhesion, rather than toxins, appears key to its pathogenicity in pulpitis.
Area of Science:
- Oral microbiology
- Dental research
- Infectious diseases
Background:
- Streptococcus anginosus and Enterococcus faecalis are key pathogens in dental abscesses and endodontic failure.
- Understanding polymicrobial infections is crucial for effective endodontic treatment and managing pulpitis.
Purpose of the Study:
- To investigate the host response to polymicrobial pulpal infections involving S. anginosus and E. faecalis.
- To determine the role of bacterial attachment and specific species in driving inflammatory responses within the dental pulp.
Main Methods:
- An ex vivo rat tooth model was used to inoculate tooth slices with S. anginosus and E. faecalis alone or in co-culture.
- Bacterial attachment was quantified, and host response was assessed via cell viability counts, RT-qPCR for inflammatory markers (TNF-α, IL-1β), and immunohistochemistry.
Main Results:
- Both single and polymicrobial infections significantly reduced pulp cell viability.
- E. faecalis exhibited higher attachment levels than S. anginosus, with a strong affinity for pulpal vasculature.
- E. faecalis infection, particularly in polymicrobial settings, led to the greatest increase in TNF-α and IL-1β expression, localized to vasculature and odontoblasts.
Conclusions:
- E. faecalis plays a significant role in driving inflammation in polymicrobial dental pulp infections.
- The pathogenicity of E. faecalis in pulpitis appears linked to its superior ability to adhere to pulpal vasculature, rather than solely relying on secreted factors.
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