Department of Biological Sciences, Bauru School of Dentistry, University of São Paulo, Bauru, SP, Brazil.
J Clin Periodontol. 2010 Mar;37(3):248-54. doi: 10.1111/j.1600-051X.2009.01531.x.
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.
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.
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)-1beta in the periodontal tissue of TLR4(-/-) mice.
The results of this study highlighted the role of TLR4 in controlling A. actinomycetemcomitans infection.
伴放线放线杆菌是一种口腔革兰氏阴性菌，可促进牙周炎的进展。伴放线放线杆菌的分离抗原可通过 Toll 样受体 (TLR) 激活固有免疫细胞。在这项研究中，我们评估了 TLR4 在控制伴放线放线杆菌感染中的作用。
我们研究了调节 TLR4(-/-) 小鼠伴放线放线杆菌诱导的牙周病结果的机制。通过 ELISA 评估细胞因子的产生。通过计数每克组织的菌落形成单位来确定细菌负荷。
结果表明，TLR4 缺陷型小鼠在伴放线放线杆菌感染后发生的牙周炎较轻，其特征为骨丢失和炎症细胞向牙周组织迁移明显减少。然而，TLR4 的缺失促进了伴放线放线杆菌的传播。TLR4(-/-) 小鼠的牙周组织中髓过氧化物酶活性降低。我们观察到 TLR4(-/-) 小鼠牙周组织中肿瘤坏死因子-α (TNF-α) 和白细胞介素 (IL)-1β 的产生显著减少。
这项研究的结果强调了 TLR4 在控制伴放线放线杆菌感染中的作用。
