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The essential role of toll like receptor‐4 in the control of Aggregatibacter actinomycetemcomitans infection in mice
Author(s) -
Lima Hayana Ramos,
Gelani Valéria,
Fernandes Ana Paula,
Gasparoto Thaís Helena,
Torres Sérgio Aparecido,
Santos Carlos Ferreira,
Garlet Gustavo Pompermaier,
Da Silva João Santana,
Campanelli Ana Paula
Publication year - 2010
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/j.1600-051x.2009.01531.x
Subject(s) - aggregatibacter actinomycetemcomitans , tlr4 , periodontitis , immunology , toll like receptor , innate immune system , medicine , microbiology and biotechnology , immune system , tumor necrosis factor alpha , biology , porphyromonas gingivalis
Lima HR, Gelani V, Fernandes AP, Gasparoto TH, Torres SA, Santos CF, Garlet GP, da Silva JS, Campanelli AP. The essential role of toll like receptor‐4 in the control of Aggregatibacter actinomycetemcomitans infection in mice. J Clin Periodontol 2010; 37: 248–254. doi: 10.1111/j.1600‐051X.2009.01531.x. 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‐ α ) and interleukin (IL)‐1 β in the periodontal tissue of TLR4 −/− mice. Conclusion: The results of this study highlighted the role of TLR4 in controlling A. actinomycetemcomitans infection.