TY - JOUR
T1 - The role of toll-like receptor 2 in the recognition of aggregatibacter actinomycetemcomitans
AU - Gelani, Valéria
AU - Fernandes, Ana Paula
AU - Gasparoto, Thaís Helena
AU - Garlet, Thiago Pompermaier
AU - Cestari, Tânia Mary
AU - Lima, Hayana Ramos
AU - Ramos, Erivan Schnaider
AU - De Souza Malaspina, Tatiana Salles
AU - Santos, Carlos Ferreira
AU - Garlet, Gustavo Pompermaier
AU - Da Silva, João Santana
AU - Campanelli, Ana Paula
N1 - Copyright:
Copyright 2012 Elsevier B.V., All rights reserved.
PY - 2009/12
Y1 - 2009/12
N2 - Background: Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans) is a Gram-negative bacterium present in the oral cavity and is usually associated with localized aggressive periodontitis. Isolated antigens from A. actinomycetemcomitans can activate innate immune cells through Toll-like receptors (TLRs), which are molecules that recognize structural components conserved among microorganisms. In this study, we evaluate the role of TLR2 in the recognition of A. actinomycetemcomitans. Methods: Macrophages and neutrophils from knockout mice with targeted disruption of TLR2 (TLR2 -/- mice) and wild-type mice were collected and used for the subsequent assays. The production of cytokines and chemokines was evaluated by enzyme-linked immunosorbent assay (ELISA), and the presence of apoptotic cells was determined by flow cytometry. In addition, the mechanisms that modulate the outcome of A. actinomycetemcomitans-induced periodontal disease in TLR2 -/- mice were examined. Results: The results show that TLR2-deficientmice developed more severe periodontitis after A. actinomycetemcomitans infection, characterized by significantly higher bone loss and inflammatory cell migration to periodontal tissues. The inflammatory cell influx into the peritoneal cavities of TLR2 -/- mice was three-fold lower than that observed for the littermate controls.Asignificantly diminished production of the cytokines tumor necrosis factor-alpha and interleukin-1β as well as the chemokine CC-ligand-5 in the peritoneal cavities of TLR2 -/- mice was observed. In addition, a high frequency of apoptotic cells in the inflammatoryexudates fromTLR2 -/- micewasobserved. Phagocytosis and nitric oxide production was diminished in cells from TLR2 -/- mice, facilitating the dissemination of the pathogen to the spleen. Conclusion: The results of this study highlight the involvment of TLR2 in recognizing A. actinomycetemcomitans and its essential role in controlling A. actinomycetemcomitans infection. J Periodontol 2009;80:2010-2019.
AB - Background: Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans) is a Gram-negative bacterium present in the oral cavity and is usually associated with localized aggressive periodontitis. Isolated antigens from A. actinomycetemcomitans can activate innate immune cells through Toll-like receptors (TLRs), which are molecules that recognize structural components conserved among microorganisms. In this study, we evaluate the role of TLR2 in the recognition of A. actinomycetemcomitans. Methods: Macrophages and neutrophils from knockout mice with targeted disruption of TLR2 (TLR2 -/- mice) and wild-type mice were collected and used for the subsequent assays. The production of cytokines and chemokines was evaluated by enzyme-linked immunosorbent assay (ELISA), and the presence of apoptotic cells was determined by flow cytometry. In addition, the mechanisms that modulate the outcome of A. actinomycetemcomitans-induced periodontal disease in TLR2 -/- mice were examined. Results: The results show that TLR2-deficientmice developed more severe periodontitis after A. actinomycetemcomitans infection, characterized by significantly higher bone loss and inflammatory cell migration to periodontal tissues. The inflammatory cell influx into the peritoneal cavities of TLR2 -/- mice was three-fold lower than that observed for the littermate controls.Asignificantly diminished production of the cytokines tumor necrosis factor-alpha and interleukin-1β as well as the chemokine CC-ligand-5 in the peritoneal cavities of TLR2 -/- mice was observed. In addition, a high frequency of apoptotic cells in the inflammatoryexudates fromTLR2 -/- micewasobserved. Phagocytosis and nitric oxide production was diminished in cells from TLR2 -/- mice, facilitating the dissemination of the pathogen to the spleen. Conclusion: The results of this study highlight the involvment of TLR2 in recognizing A. actinomycetemcomitans and its essential role in controlling A. actinomycetemcomitans infection. J Periodontol 2009;80:2010-2019.
KW - Apoptosis
KW - Cytokines
KW - Neutrophils
KW - Periodontitis
KW - Phagocytosis
KW - Toll-like receptors
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UR - http://www.scopus.com/inward/citedby.url?scp=72749103216&partnerID=8YFLogxK
U2 - 10.1902/jop.2009.090198
DO - 10.1902/jop.2009.090198
M3 - Article
C2 - 19961384
AN - SCOPUS:72749103216
SN - 0022-3492
VL - 80
SP - 2010
EP - 2019
JO - Journal of periodontology
JF - Journal of periodontology
IS - 12
ER -