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Updated: May 26, 2026
Inducing Apical Periodontitis in Mice
Published on: August 6, 2019
Cytokine expression in response to root canal infection in gnotobiotic mice
K F Maciel1, L C Neves de Brito, W L F Tavares
1Departamento de Odontologia Restauradora, Faculdade de Odontologia, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Aim:
To examine cytokine expression profiles during periapical lesion development in response to synergetic human pathogens in a gnotobiotic mouse model.
Methodology:
Human strains of Fusobacterium nucleatum and Peptostreptococcus prevotii were inoculated into the root canals of germ-free mice in either mono- or bi-association. Animals were killed 7 and 14 days after infection, and periapical tissues were collected. mRNA expression of the cytokines IFN-γ, TNF-α, Receptor activator of nuclear factor kappa-B ligand (RANKL), IL-10, IL-4 and transforming growth factor β (TGF-β) was assessed using real-time PCR. Levene's test was used to assess the equality of variance of the data, whereas a t-test for independent samples was used to evaluate the significance of the differences between groups (P < 0.05).
Results:
The mRNA expression of IFN-γ and TNF-α was up-regulated by F. nucleatum during the acute (day 7) and chronic phase (day 14) of periapical lesion development. However, in bi-infection the expression of IFN-γ and TNF-α were effectively absent at both time-points. RANKL mRNA expression was down-regulated during dual infection at the chronic phase. As IL-4 expression was similar at both time-points, IL-4 does not appear to be involved in the periapical response to these bacterial strains. IL-10 was up-regulated during the chronic phase by mono-infection with either F. nucleatum or P. prevotii. Dual infection increased TGF-β mRNA expression on day 7, which paralleled the decrease in IFN-γ and TNF-α mRNA levels at the same time-point. F. nucleatum increased TGF-β mRNA expression during the chronic phase.
Conclusion:
Cytokine profiles depend on the nature of the bacterial challenge. Both TGF-β and IL-10 appeared to be regulating the proinflammatory cytokine responses at both time-points of the periapical immune response.
Insights
Cytokine profiles in periapical lesions vary with bacterial challenge. Interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β) appear to regulate inflammatory responses to Fusobacterium nucleatum and Peptostreptococcus prevotii.
Area of Science:
- Oral microbiology
- Immunology
- Pathology
Background:
- Periapical lesions result from polymicrobial infections.
- Understanding host immune response to specific pathogens is crucial.
Purpose of the Study:
- To investigate cytokine expression profiles during periapical lesion development.
- To analyze the impact of synergistic human pathogens (Fusobacterium nucleatum and Peptostreptococcus prevotii) in a gnotobiotic mouse model.
Main Methods:
- Gnotobiotic mice were inoculated with F. nucleatum and P. prevotii (mono- or bi-association).
- Periapical tissues were collected at 7 and 14 days post-infection.
- Real-time PCR was used to quantify mRNA expression of cytokines: IFN-γ, TNF-α, RANKL, IL-10, IL-4, and TGF-β.
Main Results:
- F. nucleatum upregulated IFN-γ and TNF-α in mono-infection; these were absent in bi-infection.
- RANKL was downregulated in bi-infection during the chronic phase.
- IL-10 was upregulated by mono-infection; dual infection increased TGF-β, correlating with decreased IFN-γ and TNF-α.
Conclusions:
- Cytokine expression profiles are dependent on the specific bacterial challenge.
- IL-10 and TGF-β play regulatory roles in the periapical immune response to these pathogens.
