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Is a fatty acid transporter, CD36, involved in Mycobacterium tuberculosis infection?

Research Project

Project/Area Number 14572174
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Laboratory medicine
Research InstitutionHOKKAIDO UNIVERSITY

Principal Investigator

CHIBA Hitoshi  Hokkaido University Hospital, 医学部・歯学部附属病院, 講師 (70197622)

Project Period (FY) 2002 – 2003
Project Status Completed (Fiscal Year 2003)
Budget Amount *help
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 2003: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000)
Keywordstuberculosis / fatty acid / CD36 / macrophage
Research Abstract

CD36 is an oxidized LDL receptor and a fatty acid transporter expressed in various tissues and cells, including macrophages. Since M.tuberculosis requires fatty acid in its entry into macrophages, intracellular growth, and escape from lysosomes. In the present study, possible role of CD36 in M.tuberculosis infection to human macrophages was examined. Monocyte-derived macrophages from normal and CD36-negative subjects were infected with M.tuberculosis in vitro. The susceptibility to M.tuberculosis infection was not different between normal and CD36-negative subjects. Further, monoclonal anti-CD36 antibody did not show significant suppressive effect on the infection of M.tuberculosis to macrophages. Confocal laser microscopy did not show any significant relation between CD36 and M.tuberculosis. Thus, no definite relation between CD36 and M.tuberculosis infection was observed in this stud. However, the infection appeared to change macrophageal fatty acid composition, and also the expression levels of CD36 and PPARgamma genes. Since he both genes have significant effects on intracellular fatty metabolism and transport, possible indirect role of CD36 in M.tuberculosis infection to macrophages remains to be tested.

Report

(3 results)
  • 2003 Annual Research Report   Final Research Report Summary
  • 2002 Annual Research Report

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Published: 2002-04-01   Modified: 2016-04-21  

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