Murine Experimental Root Canal Infection: Cytokine Expression in Response to F. nucleatum and E. faecalis.

Andressa Lamari Reis,Universidade Federal De Minas Gerais, Brazil ,Ricardo Reis Oliveira,Leda Quércia Vieira,Luiz De Macêdo Farias,Warley Luciano Fonseca Tavares,Thamyris Duque Silva Saldanha,Antônio Paulino Ribeiro Sobrinho

doi:10.1590/0103-6440201600926

Andressa Lamari Reis, Universidade Federal De Minas Gerais, Brazil + Show 6 more

Open Access

https://doi.org/10.1590/0103-6440201600926

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Abstract

The aim of this study was to evaluate the gene expression of proinflammatory (RANKL, TNF-a and IFN-g) and regulatory (TGF-b and IL-10) cytokines as reaction to experimental infection by mono or bi-association of Fusobacterium nucleatum (ATCC 10953) and Enterococcus faecalis (ATCC 19433). F. nucleatum and E. faecalis, either in mono- or bi-association were inoculated into the root canal system (RCS) of Balb/c mice. Animals were sacrificed at 10 and 20 days after infection and periapical tissues surrounding the root were collected. The mRNA expression of the cytokines RANKL, TNF-a, IFN- g, TGF-b and IL-10 was assessed using real-time PCR. The Kruskal-Wallis test was used for statistical analysis. F. nucleatum mono-infection induced high expression of RANKL and TNF-a, while its modulation was due to IL-10. High expression of IFN-g at day 20 was up-regulated by E. faecalis and RANKL; TNF-a was up-regulated by an independent mechanism via IL-10 and TGF-b. Bi-association (F. nucleatum and E. faecalis) stimulated high expression of RANKL, TNF-a and IFN-g, which seemed to be modulated by TGF-b 20 days later. The gene expression of proinflammatory cytokines was more prominent in the earlier periods of the experimental periapical infection, which concomitantly decreased in the later period. This expression may be regulated by IL-10 and TGF-b in an infection-specific condition.

Highlights

Root canal infections lead to the development of periapical lesions
Bi-association was chosen since some strict anaerobic bacteria may be more powerful in inducing apical periodontitis when associated with other anaerobic or facultative microorganisms [1]
Pro-inflammatory (RANKL, TGF-α e IFN-γ) and regulatory (IL-10 e TGF-β) cytokine expression were assayed by qPCR

Summary

Introduction

Root canal infections lead to the development of periapical lesions. their development depends on the infecting microbiota as well as the host response [1].In polymicrobial infections, synergistic or antagonistic microbial interactions play a role in the pathogenic effects of microorganisms [2,3]. Root canal infections lead to the development of periapical lesions. Their development depends on the infecting microbiota as well as the host response [1]. Synergistic or antagonistic microbial interactions play a role in the pathogenic effects of microorganisms [2,3]. Bacterial relationships involve different associations: among Gram-negative species and between Gram-negative and Gram-positive species. The peptidoglycan cell wall of Gram-positive bacteria acts synergistically with lipopolysaccharides (LPS) of Gramnegative [4], complicating even more the antigenicity of the endodontic content. Former researches have clearly demonstrated differences between Gram-positive and Gram-negative bacteria, in mono or bi-association, which induce cytokine and chemokine expression [5]

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