Journal
MICROORGANISMS
Volume 9, Issue 3, Pages -Publisher
MDPI
DOI: 10.3390/microorganisms9030622
Keywords
cytokines; epithelial cells; keratinocytes; macrophages; Aggregatibacter actinomycetemcomitans; periodontitis
Categories
Funding
- Fondo Nacional de Desarrollo Cientifico y Tecnologico (FONDECYT), Santiago, Chile [1180122]
- VRID by the Vicerrectoria de Investigacion y Desarrollo, Universidad de Concepcion, Concepcion, Chile [218.101.009-1.0]
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This study evaluated the response of oral keratinocytes and macrophages to Aggregatibacter actinomycetemcomitans, finding that different serotypes of the bacteria induced increased expression of cytokines and related molecules in the cells at various time points after infection. Keratinocytes and macrophages contribute to early inflammation in periodontitis, acting as the first signal for immune cell recruitment and modulation of immune responses.
Background: Periodontitis is a chronic inflammatory disease associated with a dysbiotic biofilm. Many pathogens have been related with its progression and severity, one of which is Aggregatibacter actinomycetemcomitans, a Gram-negative bacteria with seven serotypes (a-g) according with the structure of its LPS, with serotype b defined as the most virulent compared with the other serotypes. The aim of this study was to evaluate the response of oral keratinocytes and macrophages to A. actinomycetemcomitans. Methods: Oral keratinocytes (OKF6/TERT2) and macrophages (THP-1) were infected with A. actinomycetemcomitans serotypes a, b and c. The expression of IL-1 beta, IL-6, IL-8, IL-18, TNF-alpha, MMP-9, RANKL, TLR-2, TLR-4, TLR-6, thymic stromal lymphopoietin (TSLP), and ICAM-1 was evaluated by qPCR at 2 and 24 h after infection. Results: An increase in the expression of these molecules was induced by all serotypes at both times of infection, with macrophages showing higher levels of expression at 24 h compared to epithelial cells in which the highest levels were observed in the first hours after infection. Conclusions: Keratinocytes and macrophages contribute to the inflammation in periodontitis from the early stages of infection, producing the first waves of cytokines, acting as the first signal for professional immune cell recruitment and modulation of more specific immune responses.
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