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2019 Fiscal Year Final Research Report

Molecular analyses of the mechanisms of severe pneumococcal pneumonia and search for control method using neutrophil immunity

Research Project

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Project/Area Number 17H04367
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Morphological basic dentistry
Research InstitutionNiigata University

Principal Investigator

Terao Yutaka  新潟大学, 医歯学系, 教授 (50397717)

Co-Investigator(Kenkyū-buntansha) 土門 久哲  新潟大学, 医歯学系, 准教授 (00594350)
前川 知樹  新潟大学, 医歯学系, 研究教授 (50625168)
Project Period (FY) 2017-04-01 – 2020-03-31
Keywords好中球
Outline of Final Research Achievements

It has long been known that pneumococci perform autolysis. In addition, recent pathological diagnosis has revealed that a large amount of neutrophils infiltrate human pneumococcal infection sites. Furthermore, it has been reported that the infectious disease specialists in Japan and overseas can reduce the severity of pneumonia by administering an inhibitor of neutrophil endogenous protease. However, there was no research paper that integrated and elucidated them. Therefore, we carried out the mass spectrometric analysis on the molecular mechanism by which pneumonia becomes severe from two directions: the pneumococcal side and the human neutrophil side. Then, we integrated the elucidation data of the pneumococcal side and the human side, and identified a group of molecular candidates involved in the severity of pneumonia

Free Research Field

口腔細菌学

Academic Significance and Societal Importance of the Research Achievements

誤嚥性肺炎を含めた肺炎は,耐性菌の出現と高齢社会を迎え増加・重症化している.2016年以降,日本政府および国連が,具体名を挙げて肺炎を人類の最脅威のひとつに定義している.WHOならびに国連の最新試算では,抗菌薬以外の対策を考案できなければ,2050年以降は毎年1000万人の死者が出ると予測されている.本研究の結果,肺炎球菌だけが好中球を敢えて周囲に集積させて好中球を傷害し,同細胞の内容物を利用して感染拡大を行うユニークな知見を掴んだ.今後は本研究成果に加え,好中球を利用する肺炎球菌の病原機構を詳細解析し,その制御法へと繋げることができる.

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Published: 2021-02-19  

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