Gingipains Inactivate a Cell Surface Ligand on Porphyromonas gingivalis That Induces TLR2‐ and TLR4‐Independent Signaling
Gingipains Inactivate a Cell Surface Ligand on Porphyromonas gingivalis That Induces TLR2‐ and TLR4‐Independent Signaling
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牙龈蛋白酶使牙龈卟啉单胞菌上诱导 TLR2 和 TLR4 独立信号传导的细胞表面配体失活
DOI：
10.1111/j.1348-0421.2006.tb03799.x
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发表时间：
2006
影响因子：
2.6
通讯作者：
K. Nakayama
中科院分区：
文献类型：
--
作者：
M. Kishimoto;A. Yoshimura;M. Naito;K. Okamoto;Kenji Yamamoto;D. Golenbock;Y. Hara;K. Nakayama
精氨酸特异性牙龈菌蛋白酶和赖氨酸特异性牙龈菌蛋白酶是牙龈卟啉单胞菌产生的两种主要半胱氨酸蛋白酶。为了阐明牙龈卟啉菌蛋白酶在牙龈卟啉菌和先天免疫系统之间相互作用中的作用，用野生型或牙龈卟啉菌蛋白酶缺陷型牙龈卟啉菌细胞刺激表达TLR 2或TLR 4的CHO报告细胞，并检查这些细胞中核因子-κB的活化。虽然CHO/CD 14细胞和7.19细胞（一种源自CHO/CD 14细胞的MD-2缺陷型突变体）对野生型牙龈卟啉单胞菌没有反应，但它们对牙龈卟啉单胞菌蛋白酶缺陷型牙龈卟啉单胞菌有反应。另一方面，CHO/CD 14/TLR 2细胞对野生型和牙龈卟啉单胞菌蛋白酶缺陷型牙龈卟啉单胞菌都有反应。这些结果表明，牙龈卟啉菌蛋白酶对牙龈卟啉单胞菌的TLR 2依赖性信号传导没有影响，但对CHO细胞中的TLR 2和TLR 4非依赖性信号传导具有抑制作用。事实上，在用牙龈菌蛋白酶处理细菌细胞后，牙龈菌蛋白酶缺陷型牙龈卟啉单胞菌诱导7.19细胞活化的活性减弱。接下来，我们从牙龈卟啉单胞菌蛋白酶缺陷型牙龈卟啉单胞菌中部分纯化了激活7.19细胞的细菌细胞组分。部分纯化的组分的活性通过用热或牙龈卟啉菌蛋白酶处理而减少。还值得注意的是，抗CD 14 mAb抑制了部分纯化组分诱导的7.19细胞活化。这些结果表明，牙龈卟啉单胞菌中能够诱导TLR 2和TLR 4非依赖性信号传导的组分在被CD 14识别之前被牙龈卟啉菌蛋白酶灭活。这些组分的失活将有助于牙龈卟啉单胞菌逃避天然免疫系统。
Arginine‐specific gingipain and lysine‐specific gingipain are two major cysteine proteinases produced by Porphyromonas gingivalis. To clarify the role of gingipains in the interaction between P. gingivalis and the innate immune system, CHO reporter cells expressing TLR2 or TLR4 were stimulated with wild‐type or gingipain‐deficient P. gingivalis cells and activation of nuclear factor‐κB in these cells was examined. While CHO/CD14 cells and 7.19 cells, an MD‐2‐defective mutant derived from CHO/CD14 cells, failed to respond to wild‐type P. gingivalis, they responded to gingipain‐deficient P. gingivalis. On the other hand, CHO/CD14/TLR2 cells responded to both wild‐type and gingipain‐deficient P. gingivalis. These results suggested that gingipains have no effects on TLR2‐dependent signaling from P. gingivalis but have inhibitory effects on TLR2‐ and TLR4‐independent signaling in CHO cells. Indeed, the activity of gingipain‐deficient P. gingivalis to induce the activation of 7.19 cells was diminished after treatment of the bacterial cells with gingipains. We next partially purified bacterial cell components activating 7.19 cells from gingipain‐deficient P. gingivalis. The activity of the partially purified components was diminished by treatment with heat or gingipains. It is also noteworthy that anti‐CD14 mAb inhibited the activation of 7.19 cells induced by the partially purified components. These results indicated that the components of P. gingivalis that were able to induce TLR2‐ and TLR4‐independent signaling were inactivated by gingipains before being recognized by CD14. The inactivation of the components would be helpful for P. gingivalis to escape from the innate immune system.
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影响因子：
4.4
作者：
A. Yoshimura;E. Lien;R. Ingalls;E. Tuomanen;R. Dziarski;D. Golenbock
通讯作者：
A. Yoshimura;E. Lien;R. Ingalls;E. Tuomanen;R. Dziarski;D. Golenbock
儿童牙龈卟啉单胞菌感染与局部及全身因素的关系
影响因子：
4.3
作者：
Bimstein,Enrique;Sapir,Shabetai;Houri-Haddad,Yael;Dibart,Serge;VanDyke,ThomasE;Shapira,Lior
通讯作者：
Shapira,Lior
牙龈卟啉单胞菌半胱氨酸蛋白酶（gingipains）对白细胞介素 6 受体（IL-6R）进行蛋白水解，抑制白细胞介素 6 介导的细胞活化。
影响因子：
3.8
作者：
Oleksy,Aneta;Banbula,Agnieszka;Bugno,Marcin;Travis,James;Potempa,Jan
通讯作者：
Potempa,Jan
脂多糖报告细胞系的构建及其在识别内毒素（而非 TNF-α）信号转导缺陷突变体中的应用。
DOI：
--
发表时间：
1998
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Delude,RL;Yoshimura,A;Ingalls,RR;Golenbock,DT
通讯作者：
Golenbock,DT