4.5 Article

Immune Response Profile against Persistent Endodontic Pathogens Candida albicans and Enterococcus faecalis In Vitro

期刊

JOURNAL OF ENDODONTICS
卷 41, 期 7, 页码 1061-1065

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.joen.2015.02.016

关键词

Apical periodontitis; bone resorption; Candida albicans; endodontics; Enterococcus faecalis

资金

  1. Universidade Catolica de Brasilia (UCB)
  2. Conselho Nacional de Desenvolvimento Tecnologico (CNPq) [UNIVERSAL - CNPQ - 470477/2012-1]
  3. Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
  4. Fundacao de Amparo do Distrito Federal (FAPDF)

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Introduction: Persistent microorganisms such as Candida albicans and Enterococcus faecalis might be directly related to endodontic treatment failure. The host response to these microorganisms impairs the reestablishment of intraradicular and periradicular health. Methods: The present investigation evaluated the expression of inflammatory mediators produced by RAW 264.7 cells in the presence of heat-killed antigens (HK) C. albicans and E. faecalis. Cultures of RAW cells were stimulated with both antigens in the presence or absence of recombinant interferon (rIFN)-gamma. Parameters of cell viability, production of nitric oxide (NO), as well as the synthesis of interleukin (IL)-1 alpha, IL-6, IL-10, IL-12, monocyte chemotactic protein-1, and tumor necrosis factor (TNF)-alpha were analyzed. Results: Results demonstrated that cell viability was especially reduced in antigens and rIFN-gamma-stimulated groups. Groups stimulated with HK C. albicans upregulated IL-10 production. Otherwise, the addition of rIFN-gamma to HK C. albicans upregulated TNF-alpha and NO production. Groups stimulated with HK E. faecalis upregulated TNF-alpha production. HK E. faecalis and rIFN-gamma upregulated INF-alpha and NO synthesis. The production of other cytokines remained unchanged by all stimuli. Conclusions: Knowledge regarding the host mechanism of response to microorganisms that perpetuate endodontic infection,and the periradicular lesions can contribute to optimization of endodontic therapy. The mentioned inflammatory mediators and virulence factors involved in endodontic failure might guide lesion progression and also be targets in the development of disinfectant and immunomodulatory agents.

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