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2017 Fiscal Year Final Research Report

Elucidation of mechanisms that unknown component of Mycobacterium leprae induced foamy macrophages

Research Project

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Project/Area Number 15K19097
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Bacteriology (including mycology)
Research InstitutionTeikyo University

Principal Investigator

TANIGAWA KAZUNARI  帝京大学, 薬学部, 助教 (10443110)

Co-Investigator(Renkei-kenkyūsha) Suzuki Koichi  帝京大学, 医療技術学部臨床検査学科, 教授 (20206478)
Project Period (FY) 2015-04-01 – 2018-03-31
Keywordsらい菌 / トリアシルグリセロール / GPAT3
Outline of Final Research Achievements

Mycobacterium leprae (M. leprae), the causative agent of leprosy, parasitizes within host macrophages. M. leprae lives and replicates in foamy or enlarged phagosomes within macrophages that are filled with lipids, which provide essential source to form cell wall of the mycobacteria. In the present study, we tried to identify lipid species accumulated following infection and to elucidate the underlying mechanisms for the lipid accumulation in M. leprae-infected macrophages. Most abundant lipid in M. leprae-infected cells was triacylglycerol (TAG). In addition, a large number of fatty acid-containing molecular species were detected in TAG. Expression of GPAT3, a key enzyme in the fatty acid catalysis, was significantly increased in M. leprae infected cells. Further elucidation of specific lipid components in the host cell during infection will establish the mechanism of intracellular survival of M. leprae.

Free Research Field

脂質生化学

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Published: 2019-03-29  

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