Evaluation of chemokines and receptors in gnotobiotic root canal infection by F. nucleatum and E. faecalis

Abstract

The present study aims to evaluate the longitudinal effects of induced experimental infections in gnotoxenic animals on the expression of inflammatory chemokines and their receptors in periradicular tissues. The null hypothesis tested was that Enterococcus faecalis and Fusobacterium nucleatum had no effect on CCR5, CCL5, CXCL10, CCL2/MCP-1, CXCR2 and CCR1 expression. Two groups of five animals (n = 5) aged between 8 and 12 weeks were used in this study. The animals were anaesthetized, and coronary access was performed in the first molar on the right and left sides. Microorganisms were inoculated into the left molar, and the right molar was sealed without contamination to function as a control. Animals were sacrificed 7 and 14 days after infection, and periapical tissues were collected. The cytokine mRNA expression levels were assessed using realtime PCR. The chemokine mRNA expression levels demonstrated that the experimental infection was capable of inducing increased chemokine expression on day 7 compared to that on day 14, except for CCR5 and CCL5, which showed no changes. The gnotoxenic animal model proved to be effective and allowed evaluation of the immune response against a known infection. Additionally, this study demonstrates that gene expression of chemokines and their receptors against the experimental infection preferentially prevailed during the initial phase of induction of the periradicular alteration (i.e., on day 7 post-infection).

A Pilot Study of Chronological Microbiota Changes in a Rat Apical Periodontitis Model

“…Although rat apical periodontitis models to investigate endodontic infection have been introduced, most studies have focused on periapical lesions and histologic changes at a specific time point [ 14 , 22 ], and the chronological changes in the microbiota together with radiologic and histologic analyses has been poorly studied. Notably, there are some previous reports available on the induction of murine apical periodontitis by Enterococcus faecalis or Fusobacterium nucleatum [ 23 , 24 ] and rat chronic apical periodontitis by Porphyromonas gingivalis or E. faecalis [ 25 ]. Nonetheless, those reports have seemingly only limited applicability for the comprehensive understanding of the role of microbial communities responsible for the disease progress.…”