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诱导型一氧化氮合酶的缺乏会导致牙龈卟啉单胞菌诱导的组织损伤。

Deficiency of iNOS contributes to Porphyromonas gingivalis-induced tissue damage.

作者信息

Alayan J, Ivanovski S, Gemmell E, Ford P, Hamlet S, Farah C S

机构信息

Oral Biology and Pathology, School of Dentistry, University of Queensland, Brisbane, Australia.

出版信息

Oral Microbiol Immunol. 2006 Dec;21(6):360-5. doi: 10.1111/j.1399-302X.2006.00304.x.

Abstract

Periodontitis is a chronic inflammatory disease that results in extensive soft and hard tissue destruction of the periodontium. Porphyromonas gingivalis possesses an array of virulence factors and has been shown to induce expression of inducible nitric oxide synthase (iNOS) in inflammatory cells. The aim of this study was to investigate the effect of eliminating iNOS in a murine model of P. gingivalis infection. This was achieved by utilizing a P. gingivalis-induced skin abscess model, and an alveolar bone loss model employing an oral infection of P. gingivalis in iNOS knockout mice. The results indicated that iNOS knockout mice exhibit more extensive soft tissue damage and alveolar bone loss in response to P. gingivalis infection compared to wild-type mice. The local immune response to P. gingivalis in iNOS knockout mice was characterized by increased numbers of polymorphonuclear monocytes, while the systemic immune response was characterized by high levels of interleukin-12. The iNOS is required for an appropriate response to P. gingivalis infection.

摘要

牙周炎是一种慢性炎症性疾病,可导致牙周组织广泛的软硬组织破坏。牙龈卟啉单胞菌具有一系列毒力因子,并已被证明可诱导炎症细胞中诱导型一氧化氮合酶(iNOS)的表达。本研究的目的是在牙龈卟啉单胞菌感染的小鼠模型中研究消除iNOS的作用。这是通过利用牙龈卟啉单胞菌诱导的皮肤脓肿模型以及在iNOS基因敲除小鼠中进行牙龈卟啉单胞菌口腔感染的牙槽骨丧失模型来实现的。结果表明,与野生型小鼠相比,iNOS基因敲除小鼠在受到牙龈卟啉单胞菌感染时表现出更广泛的软组织损伤和牙槽骨丧失。iNOS基因敲除小鼠对牙龈卟啉单胞菌的局部免疫反应的特征是多形核单核细胞数量增加,而全身免疫反应的特征是白细胞介素-12水平升高。iNOS是对牙龈卟啉单胞菌感染作出适当反应所必需的。

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