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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

The essential role of toll like receptor-4 in the control of Aggregatibacter actinomycetemcomitans infection in mice

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Author(s):
Lima, Hayana Ramos [1] ; Gelani, Valeria [1] ; Fernandes, Ana Paula [1] ; Gasparoto, Thais Helena [1] ; Torres, Sergio Aparecido [1] ; Santos, Carlos Ferreira [1] ; Garlet, Gustavo Pompermaier [1] ; da Silva, Joao Santana [2] ; Campanelli, Ana Paula [1]
Total Authors: 9
Affiliation:
[1] Univ Sao Paulo, Dept Biol Sci, Bauru Sch Dent, BR-17012901 Bauru, SP - Brazil
[2] Univ Sao Paulo, Dept Biochem & Immunol, Sch Med Ribeirao Preto, BR-14049 Ribeirao Preto, SP - Brazil
Total Affiliations: 2
Document type: Journal article
Source: JOURNAL OF CLINICAL PERIODONTOLOGY; v. 37, n. 3, p. 248-254, MAR 2010.
Web of Science Citations: 24
Abstract

Objective: Aggregatibacter actinomycetemcomitans is an oral Gram-negative bacterium that contributes to periodontitis progression. Isolated antigens from A. actinomycetemcomitans could be activating innate immune cells through Toll-like receptors (TLRs). In this study, we evaluated the role of TLR4 in the control of A. actinomycetemcomitans infection. Material and Methods: We examined the mechanisms that modulate the outcome of A. actinomycetemcomitans-induced periodontal disease in TLR4(-/-) mice. The production of cytokines was evaluated by ELISA. The bacterial load was determined by counting the number of colony-forming units per gram of tissue. Results: The results showed that TLR4-deficient mice developed less severe periodontitis after A. actinomycetemcomitans infection, characterized by significantly lower bone loss and inflammatory cell migration to periodontal tissues. However, the absence of TLR4 facilitated the A. actinomycetemcomitans dissemination. Myeloperoxidase activity was diminished in the periodontal tissue of TLR4(-/-) mice. We observed a significant reduction in the production of tumour necrosis factor-alpha (TNF-alpha) and interleukin (IL)-1 beta in the periodontal tissue of TLR4(-/-) mice. Conclusion: The results of this study highlighted the role of TLR4 in controlling A. actinomycetemcomitans infection. (AU)