Please use this identifier to cite or link to this item:
http://hdl.handle.net/1843/ODON-AZWKZF
Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.advisor1 | Antonio Paulino Ribeiro Sobrinho | pt_BR |
dc.contributor.referee1 | Evandro Neves Abdo | pt_BR |
dc.contributor.referee2 | Gil Moreira Júnior | pt_BR |
dc.creator | Lucas Moreira Maia | pt_BR |
dc.date.accessioned | 2019-08-14T14:13:10Z | - |
dc.date.available | 2019-08-14T14:13:10Z | - |
dc.date.issued | 2017-07-31 | pt_BR |
dc.identifier.uri | http://hdl.handle.net/1843/ODON-AZWKZF | - |
dc.description.abstract | This study aims to identify the gene expression of a new group of T lymphocytes, Th9 cells, characteristically responsible for producing IL-9 in the periradicular tissues of individuals with endodontic infections submitted to routine endodontic therapy, in the presence and absence of infection as well as the cytokines TNF-, IL-1. IL-9, INF- and IL-10 and CCL-2 / MCP-1 and CCR-6 chemokines in the periapical interstitial fluid of human root canal infections. Samples were collected immediately after cleaning and formatting procedures and 7 days later (after reduction of intracanal microbial load) to characterize the expression of these genes. Real-time polymerase chain reaction demonstrated significantly higher levels of IL-1, IL-9, INF-, TNF- and IL-10 markers at day 7 compared to day 0. In turn, the CCL-2 / MCP-1 and CCR-6 chemokines and IL- 17A cytokine showed no significant differences in mRNA expression between the 2 periods analyzed. In analyzing the clinical variation after endodontic therapy on periapical immune status, this study demonstrated that the cytokine and chemokinemediated proinflammatory response appears to be modulated in a IL-10 / IL-9 dependent manner. | pt_BR |
dc.description.resumo | Este estudo tem como objeitvo Identificar a expressao genica de um novo grupo de linfocitos T, as celulas Th9, caracteristicamente responsavel por produzirem a IL-9 nos tecidos perirradiculares de individuos portadores de infeccoes endodonticas submetidos a terapia endodontica de rotina, na presenca e ausencia de infeccao assim como as citocinas TNF-, IL-1. IL-9, INF- e IL-10 e das quimiocinas CCL-2/MCP-1 e CCR-6 no fluido intersticial periapical de infeccoes de canais radiculares humanas. As amostras foram coletadas imediatamente apos os procedimentos de limpeza e formatacao e 7dias mais tarde (apos reducao da carga microbiana intracanal) para caracterizar a expressao destes genes. A reacao em cadeia da polimerase em tempo real demonstrou niveis significativamente maiores de marcadores de IL-1, IL-9, INF-, TNF- e IL-10 no dia 7 quando comparado com ao dia 0. Por sua vez, as quimiocinas CCL-2/MCP-1 e CCR-6 e a citocina IL-17A nao apresentaram diferencas significativas na expressao de mRNA entre os 2 periodos analisados. Ao analisar a variacao clinica pos terapia endodontica sobre a condicao imune periapical, este estudo demonstrou que a resposta pro-inflamatoria mediada por citocinas e quimiocinas parece ser modulada de forma IL-10/IL-9 dependente. | pt_BR |
dc.language | Português | pt_BR |
dc.publisher | Universidade Federal de Minas Gerais | pt_BR |
dc.publisher.initials | UFMG | pt_BR |
dc.rights | Acesso Aberto | pt_BR |
dc.subject | Citocina | pt_BR |
dc.subject | TH9 | pt_BR |
dc.subject | Periodontite Apical | pt_BR |
dc.subject | Quimiocina | pt_BR |
dc.subject | Interleucina IL-9 | pt_BR |
dc.subject.other | Periodontite periapical | pt_BR |
dc.subject.other | Interleucina-9 | pt_BR |
dc.subject.other | Quimiocinas | pt_BR |
dc.subject.other | Citocinas | pt_BR |
dc.title | Papel protetor das citocinas IL-9/IL-10 em lesões perriradiculares humanas | pt_BR |
dc.type | Dissertação de Mestrado | pt_BR |
Appears in Collections: | Dissertações de Mestrado |
Files in This Item:
File | Description | Size | Format | |
---|---|---|---|---|
papel_protetor_das_citocinas_il_9il_10_em_leso_es_perriradiculares__humanas.pdf | 516.15 kB | Adobe PDF | View/Open |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.