Papel da IL-17 na imunopatogênese de lesões periapicais experimentais

• Ano de defesa: 2015
• Autor(a) principal: Kamilla Faria Maciel
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Artrite reumatóide; Lesão periapical; qPCR; Citocinas; Doenças periapicais
• Link de acesso: http://hdl.handle.net/1843/ODON-A46NP8

The infection of the root canal system will lead to consequent induction of an apical periodontitis, with many inflammatory mediators involved in this process. IL-17 has been shown to impact bone remodeling process especially in cases of arthritis, presenting at high levels. However, little is known about its role in the pathogenesis of apical periodontitis. This study aimed to evaluate the role of IL-17A in periradicular bone resorption in experimental endodontic infections in C57BL/6 and IL-17RA KO mice and the effect of these experimental infection in rheumatoid arthritis. To induce endodontic infection, strains of Porphyromonas gingivalis, Prevotella intermedia and Fusobacterium nucleatum were inoculated in the first upper left molar root canals of mice. The model of antigen-induced arthritis (AIA) was developed in both animal to further held endodontic infections. Animals were sacrificed 14 and 21 days after endodontic infection in both cases. Histological analysis was performed on the animals joints and gene expression of IL-1, TNF-, IFN-, IL-6, IL-17A, RANK, RANKL, TGF-, IL-10 and IL-4 of tooth and periapical lesions by qPCR. The AIA model could be established in IL-17RA KO and C57BL/6 mice, observing a greater joint destruction score in C57BL/6. Regarding the gene expression of cytokines, basal levels of TNF-, IFN-, TGF-, IL-10 and IL-17A as TGF-, IL-10 and IL-4 were observed in C57BL/6 and IL-17RA KO mice, respectively, in 14 and 21 days. On the 14th day, C57BL/6 mice showed a decreased expression of IL-6 and IL-17A increased. At day 21, the expression of IL-17A and IL-1 were increased, and IL-6, RANK, RANKL and IL-4 decreased. IL-17RA KO mice showed an increase of RANK on day 14 and IL-6 decreased in 14 and 21 days, where there was an increase of TNF- and IL-1 and a decrease of IFN-, IL-6, RANK and RANKL. We conclude that IL-17 is not absolutely necessary to autoimmune arthritis and the production of other pro-inflammatory mediators is sufficient to compensate its loss. The endodontic infection interfere in this expression, either in IL17RA KO and C57BL/6 mice in an IL-17 dependent manner, suggesting a possible regulation of IL-4 in these latter.