Studies on signal transduction of neutrophils from early-onset periodonititis patients

早发性牙周炎患者中性粒细胞信号转导研究

基本信息

批准号：
05454516
负责人：
KURIHARA Hidemi
金额：
$ 3.9万
依托单位：
Okayama University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1993
资助国家：
日本
起止时间：
1993 至 1994
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-05454516/
关键词：
Protein kinase C Cyclic AMP CD18 CD11 Intracellular calucium ion Phosphorylation Leukotoxin A.actinomycetemcomitans 若年性歯周炎好中球走化能プロテインキナーゼC LFA-1 FMLP cAMP

项目摘要

In this project, we analyzed themechanism of depressed neutrophil chemotaxis in patients with early-onset periodontitis from the standpoint of intracellular signal transduction mechanism. We analyzed both of depressed chemotaxis mechanism in peripheral blood neutrophil, that genetically restricted, and in a study model that might be occurred in local periodontal region as the result of host-parasite interaction. Firstly, we evaluated the association between chemotaxis of peripheral neutrophils and the progression of periodontal disease with using a new clinical parameter. We could classify the patients into two groups ; 1) patients with depressed neutrophil chemotaxis and other abnormal reaction of neutrophil and 2) patients with normal neutrophil chemotaxis and severe A.actinomycetemcomitans (Aa) infection. Former is restricted genetically and later is the result from the interaction between Aa and neutrophils. Then, we analyzed 1) the abnormal reaction of peripheral neutrophils, that … More restricted genetically, from the stand points of intracellular signal transduction and 2) the influences on signal transduction of leukocytes by leukotoxin from Aa. The main project tittles were 1. the role of neutrophil chemotaxis on advanced periodontitis, 2. depressed neutrophil chemotaxis and the signal transduction mechanism in juvenile periodontitis, i) protein kinase C activity in neutrophils from juvenile periodontitis patients, ii) the change of intracellular concentration of calcium ion with stimulation of chemoattractant, iii) the deficient expression of CD18 molecule on cell surface in early-onset periodontitis, 3. the mechanism of cytotoxity of leukotoxin from Aa. Protein kinase C activity was low in the neutrophils from juvenile periodontitis patients. Deficient CD18 expression was not caused by anomaly on the genomic DNA.leukotoxin from Aa enhances the calcium dependent phosphorylation of 110 kDa protein of HL-60 cell. Periodontitis with similar clinical status not always have the same disorder of host defensive cells even in the same family. We have to further clarify the polymorphism on mechanism of development of periodontal disease at cellular functions, bioactive molecules, and genes. Less

在这个项目中，我们从细胞内信号转导机制的角度分析了早发性牙周炎患者中性粒细胞趋化性抑郁症的效力机构。我们分析了外周血中性粒细胞中的两种抑郁趋化机制，这些机制通常受到限制，并且在宿主 - 寄生虫相互作用的结果中可能发生的研究模型中。首先，我们通过使用新的临床参数评估了外周中性粒细胞的趋化性与牙周疾病的进展之间的关联。我们可以将患者分为两组； 1）中性粒细胞和其他异常反应的患者和2）患有正常嗜中性粒细胞趋化性和严重肌张力障碍的患者（AA）感染。前者受到限制，后来是AA和中性粒细胞之间的相互作用的结果。然后，我们分析了1）外周嗜中性粒细胞的异常反应，这些反应是从细胞内信号转导的立场和2）对白细胞对白细胞信号转导的影响，从AA中的白细胞转导信号转导。钛的主要项目是1。中性粒细胞趋化性在晚期牙周炎中的作用，2。中性粒细胞趋化性降低和青少年牙周炎中的信号转导机制，i）蛋白激酶C的蛋白激酶C活性在幼年牙周炎患者中的中性粒细胞中嗜中性粒细胞中嗜中性粒细胞的粒细胞量化量的粒细胞内粒子量的变化。在早期发作牙周炎的细胞表面上，3。少年牙周炎患者的中性粒细胞中蛋白激酶C活性较低。缺乏CD18的表达不是由AA基因组DNA的异常引起的，从而增强了HL-60细胞的110 kDa蛋白的钙依赖性磷酸化。具有相似临床状况的牙周炎即使在同一家族中也并不总是患有宿主防御细胞的疾病。我们必须进一步阐明在细胞功能，生物活性分子和基因上牙周疾病发展机制的多态性。较少的