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llular信号转导机制的角度的早期牙周炎患者中嗜中性粒细胞趋化性的分析机制。宿主 - 寄生虫相互作用的结果。 sev erse a.Actinomycetemcomitans（AA）是限制的，后来是AA和中性的相互作用的结果，我们分析了外周中性粒细胞的异常反应。细胞内信号转导2）白细胞在AA中对白细胞的信号转导的影响。牙周炎，ii）tant，iii）在早期发作的牙周炎中，CD18分子的默认表达，来自AA的白细胞毒素的细胞毒素的机制低于少年牙周炎患者的中性粒细胞。基因组DNA的异常。依赖于HL-60细胞的110 kDa蛋白质的牙周毒素具有相似的临床状态细胞功能，生物活性分子和基因的牙周疾病。