Details

Autor(en) / Beteiligte

• Nishio Ayre, Wayne
• Melling, Genevieve
• Cuveillier, Camille
• Natarajan, Madhan
• Roberts, Jessica L
• Marsh, Lucy L
• Lynch, Christopher D
• Maillard, Jean-Yves
• Denyer, Stephen P
• Sloan, Alastair J
• Freitag, Nancy E.

Titel

Enterococcus faecalis Demonstrates Pathogenicity through Increased Attachment in an Ex Vivo Polymicrobial Pulpal Infection

Ist Teil von

• Infection and immunity, 2018-05, Vol.86 (5)

Ort / Verlag

United States: American Society for Microbiology

Erscheinungsjahr

2018

Link zum Volltext

Quelle

Free E-Journal (出版社公開部分のみ）

Beschreibungen/Notizen

• This study investigated the host response to a polymicrobial pulpal infection consisting of and , bacteria commonly implicated in dental abscesses and endodontic failure, using a validated rat tooth model. Tooth slices were inoculated with planktonic cultures of or alone or in coculture at / ratios of 50:50 and 90:10. Attachment was semiquantified by measuring the area covered by fluorescently labeled bacteria. Host response was established by viable histological cell counts, and inflammatory response was measured using reverse transcription-quantitative PCR (RT-qPCR) and immunohistochemistry. A significant reduction in cell viability was observed for single and polymicrobial infections, with no significant differences between infection types (∼2,000 cells/mm for infected pulps compared to ∼4,000 cells/mm for uninfected pulps). demonstrated significantly higher levels of attachment (6.5%) than alone (2.3%) and mixed-species infections (3.4% for 50:50 and 2.3% for 90:10), with a remarkable affinity for the pulpal vasculature. Infections with demonstrated the greatest increase in tumor necrosis factor alpha (TNF-α) (47.1-fold for , 14.6-fold for , 60.1-fold for 50:50, and 25.0-fold for 90:10) and interleukin 1β (IL-1β) expression (54.8-fold for , 8.8-fold for , 54.5-fold for 50:50, and 39.9-fold for 90:10) compared to uninfected samples. Immunohistochemistry confirmed this, with the majority of inflammation localized to the pulpal vasculature and odontoblast regions. Interestingly, supernatant and heat-killed treatments were unable to induce the same inflammatory response, suggesting pathogenicity in pulpitis is linked to its greater ability to attach to the pulpal vasculature.