Expressão de citocinas em resposta à infecção endodôntica experimental em camundongos isentos de germes

Abstract

Aim: To examine the cytokine expression profile during periapical lesion development in response to synergetic human pathogens in a gnotoxenic mouse model. Methodology: Fisobacterium nucleatum and Peptostreptococcus prevotii strains were isolated from a human patient and had been previously demonstrated to be synergistic in vitro, because P. prevotii triggered a significant increase in the growth of F. nucleatum. These strains were inoculated into the root canals of germ-free mice in either mono- or bi-association. Animals were sacrificed seven and 14 days after infection, and periapical tissues were collected. mRNA Expression of the cytokines IFN-, TNF-, RANKL, IL-10, IL-4, and TGF- was assessed using quantitative real-time PCR. Results: The mRNA expression of IFN- and TNF- was significantly up-regulated by F. nucleatum mono-infection during the acute and chronic phase of periapical lesion development, respectively. However, in F. nucleatum and P. prevotii bi-infection the expression of IFN- and TNF- were almost absent at both time points analysed. RANKL mRNA expression was down-regulated during the bi-infection at the chronic phase (day 14). As IL-4 expression was similar at both time points analysed, IL-4 does not appear to be involved in the periapical immune response to these bacterial strains. The immunomodulatory cytokine IL-10 was up-regulated during the chronic phase (day 14) by mono-infection with either F. nucleatum or P. prevotii. Dual infection with F. nucleatum and P. prevotii increased TGF- mRNA expression on day 7, which paralleled the decrease in IFN- and TNF- mRNA levels at the same time point. Additionally, F. nucleatum mono-infection increased TGF- mRNA expression during the chronic phase. Conclusion: We conclude that the cytokine profile expressed in periapical tissues in response to root canal infection depends on the nature of the bacterial challenge because we observed species-specific host cytokine responses. Additionally, both TGF- and IL-10 appeared to be regulating the proinflammatory cytokine responses during both the acute and chronic phases of the periapical immune response.