transforming-growth-factor-beta has been researched along with Fusobacterium-Infections* in 1 studies
1 other study(ies) available for transforming-growth-factor-beta and Fusobacterium-Infections
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Cytokine expression in response to root canal infection in gnotobiotic mice.
To examine cytokine expression profiles during periapical lesion development in response to synergetic human pathogens in a gnotobiotic mouse model.. 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).. 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.. 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. Topics: Animals; Coinfection; Cytokines; Dental Pulp Diseases; Fusobacterium Infections; Fusobacterium nucleatum; Germ-Free Life; Gram-Positive Bacterial Infections; Humans; Inflammation Mediators; Interferon-gamma; Interleukin-10; Interleukin-4; Mice; Peptostreptococcus; Periapical Diseases; RANK Ligand; Real-Time Polymerase Chain Reaction; RNA, Messenger; Time Factors; Transforming Growth Factor beta; Up-Regulation | 2012 |