Murine experimental root canal infection: cytokine expression in response to F. nucleatum and E. faecalis

• Autor(a) principal: Andressa Lamari Reis
• Data de Publicação: 2016
• Outros Autores: Ricardo Reis Oliveira, Warley Luciano Fonseca Tavares, Thamyris Duque Silva Saldanha, Luiz de Macêdo Farias, Leda Quércia Vieira, Antônio Paulino Ribeiro Sobrinho
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFMG
• Texto Completo: https://doi.org/10.1590/0103-6440201600926; http://hdl.handle.net/1843/56237; https://orcid.org/0000-0003-2077-927X; https://orcid.org/0000-0001-5481-9618; https://orcid.org/0000-0002-3598-7592
• topic: Cytokines; Gram-positive bacteria; Gram-negative bacteria; Periapical lesion; Citocinas; Bactérias gram-positivas; Bactérias gram-negativas; Cavidade pulpar

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.