Aggregatibacter actinomycetemcomitans, a potent immunoregulator of the periodontal host defense system and alveolar bone homeostasis.
Aggregatibacter actinomycetemcomitans, a potent immunoregulator of the periodontal host defense system and alveolar bone homeostasis.
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DOI：
10.1111/omi.12119
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发表时间：
2016-06
影响因子：
3.7
通讯作者：
Kirkwood KL
中科院分区：
文献类型：
--
作者：
Herbert BA;Novince CM;Kirkwood KL
伴放线菌聚集杆菌是一种牙周致病菌，长期以来与局部侵袭性牙周炎有关。其致病机制已在人类和临床前实验模型中进行了研究。虽然A.放线菌共生放线菌（Actinomycetemcomitans）的毒力因子表达存在差异，A.伴随放线菌的致死性膨胀毒素（CDT）、白细胞毒素和脂多糖（LPS）在调节宿主免疫应答的背景下已被最广泛地研究。在口腔中定植和附着后，A.伴随放线菌利用CDT、白细胞毒素和LPS来逃避宿主的先天防御机制并驱动病理生理炎症反应。这种超生理的免疫反应状态扰乱正常的牙周组织重塑/周转，并最终对牙周组织稳态产生分解代谢作用。在这篇综述中，我们将宿主反应分为两个系统：非造血和造血。非造血屏障包括启动先天免疫宿主应答的上皮和成纤维细胞。造血系统包含淋巴和骨髓来源的细胞谱系，其负责扩大免疫应答并驱动局部牙周微环境中的病理生理炎症状态。效应系统和信号转导途径激活和利用响应A。放线菌共生菌将讨论进一步描绘免疫细胞机制，在A。伴放线菌感染最后，我们将讨论A.放线菌共生菌和解剖平衡破骨细胞-成骨细胞介导的骨重建的分解代谢破坏，其随后导致净牙槽骨损失。
Aggregatibacter actinomycetemcomitans is a perio-pathogenic bacteria that has long been associated with localized aggressive periodontitis. The mechanisms of its pathogenicity have been studied in humans and pre-clinical experimental models. Although different serotypes of A. actinomycetemcomitans have differential virulence factor expression, A. actinomycetemcomitans cytolethal distending toxin (CDT), leukotoxin, and lipopolysaccharide (LPS) have been most extensively studied in the context of modulating the host immune response. Following colonization and attachment in the oral cavity, A. actinomycetemcomitans employs CDT, leukotoxin, and LPS to evade host innate defense mechanisms and drive a pathophysiologic inflammatory response. This supra-physiologic immune response state perturbs normal periodontal tissue remodeling/turnover and ultimately has catabolic effects on periodontal tissue homeostasis. In this review, we have divided the host response into two systems: non-hematopoietic and hematopoietic. Non-hematopoietic barriers include epithelium and fibroblasts that initiate the innate immune host response. The hematopoietic system contains lymphoid and myeloid-derived cell lineages that are responsible for expanding the immune response and driving the pathophysiologic inflammatory state in the local periodontal microenvironment. Effector systems and signaling transduction pathways activated and utilized in response to A. actinomycetemcomitans will be discussed to further delineate immune cell mechanisms during A. actinomycetemcomitans infection. Finally, we will discuss the osteo-immunomodulatory effects induced by A. actinomycetemcomitans and dissect the catabolic disruption of balanced osteoclast-osteoblast mediated bone remodeling, which subsequently leads to net alveolar bone loss.