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The analysis of the disease-causing gene of the tubercle bacillus and fundamental examination of tuberculosis attack control of the candidate new vaccine strain

Research Project

Project/Area Number 17590794
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Respiratory organ internal medicine
Research InstitutionNagasaki University

Principal Investigator

MIYAZAKI Yoshitsugu  Nagasaki University, Hospital of Medicine and Dentistry, Lecturer (00311861)

Co-Investigator(Kenkyū-buntansha) KOHNO Shigeru  Nagasaki University, Graduate School of Biomedical Sciences, Professor (80136647)
Project Period (FY) 2005 – 2006
Project Status Completed (Fiscal Year 2006)
Budget Amount *help
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 2006: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Keywordstuberculosis / latent infection / macrophage / NO / RNI / ctpF
Research Abstract

The tuberculosis attracts attention as reemerging infectious disease in late year. 60% of the tuberculosis patient are senior citizens in Japan. The most them are past infection patients. and it is thought as follows, and, as for becoming sick through a life among tuberculosis infection patients, it is thought that a tuberculosis patient equal to or less than 10% has tuberculosis for a life. The macrophage is important as host defense mechanism of the tuberculosis infection. There is NO (nitric oxide) and RNI (reactive nitrogen intermediates) in one of the defense mechanism of a host against tuberculosis. We got the research finding that a ctp F gene may participate in a tubercle bacillus greatly as genetic mechanism of the escape mechanism from this defense mechanism. Our object of this research is the confirmation of this result and elucidation of a concrete function of these genes. We knocked out of ctp F gene by allelic exchange method to make gene deficit strain. We examine influence of the knock out strain revealed by NO and RNI in vitro and compare it with a wild strains. In addition, we let these knock outs strain infect with human THP-1 macrophages and compare knock out strain with wild strains and examine the change of the number of viable bacteria, the viable or death of the cell, and an apoptosis instruction over time. In the future, we perform in vivo experiments with mice.

Report

(3 results)
  • 2006 Annual Research Report   Final Research Report Summary
  • 2005 Annual Research Report

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Published: 2005-04-01   Modified: 2016-04-21  

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