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

• Published in: Journal of endodontics Vol. 41; no. 7; pp. 1061 - 1065
• Main Authors: Lima, Stella Maris de Freitas, MSc, Sousa, Maurício Gonçalves da Costa, Freire, Mirna de Souza, MSc, Almeida, Jeeser Alves de, PhD, Cantuária, Ana Paula de Castro, DSc, Silva, Thaís Angélica Machado e, DDS, Freitas, Camila Guimarães de, MSc, Dias, Simoni Campos, PhD, Franco, Octávio Luiz, PhD, Rezende, Taia Maria Berto, PhD
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.07.2015
• Subjects: Animals; Antigens, Bacterial - immunology; Antigens, Fungal - immunology; Apical periodontitis; Bone Resorption; Candida albicans; Candida albicans - immunology; Cytokines - biosynthesis; Dentistry; Endocrinology & Metabolism; endodontics; Enterococcus faecalis; Enterococcus faecalis - immunology; Humans; Interferon-gamma - metabolism; Mice; Nitric Oxide - metabolism; Periapical Periodontitis - immunology; Periapical Periodontitis - microbiology; RAW 264.7 Cells; Candida albicans; endodontics; Enterococcus faecalis; Apical periodontitis; bone resorption
• ISSN: 0099-2399; 1878-3554
• DOI: 10.1016/j.joen.2015.02.016

Abstract 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)-γ. Parameters of cell viability, production of nitric oxide (NO), as well as the synthesis of interleukin (IL)-1α, IL-6, IL-10, IL-12, monocyte chemotactic protein-1, and tumor necrosis factor (TNF)-α were analyzed. Results Results demonstrated that cell viability was especially reduced in antigens and rIFN-γ–stimulated groups. Groups stimulated with HK C. albicans upregulated IL-10 production. Otherwise, the addition of rIFN-γ to HK C. albicans upregulated TNF-α and NO production. Groups stimulated with HK E. faecalis upregulated TNF-α production. HK E. faecalis and rIFN-γ upregulated TNF-α 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.