2003 Fiscal Year Final Research Report Summary
Modulation of human gp91 ^<phox> gene expression by rickettsia infection
| Project/Area Number |
14570240
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Bacteriology (including Mycology)
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| Research Institution | The Institute of Tropical Medicine, Nagasaki University |
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Principal Investigator |
NAKAMURA Michio Institute of Tropical Medicine, Nagasaki University, Department of Host-Defense Biochemistry, Professor, 熱帯医学研究所, 教授 (30091276)
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| Project Period (FY) |
2002 – 2003
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| Keywords | Ehrlihia / Rickettsia / gp91^<phox> / NADPH oxidase / p47^<phox> / Superoxide |
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| Research Abstract |
To escape from reactive oxygen species generated in response to infection, intracellular pathogens, such as Salmonellae and Anaplasma phagocytophilum, can modulate the expression and distribution of the phagocyte NADPH oxidase components.
In the present study, we analyzed the effect of Ehrlichia chaffeensis infection on the ability of human monocytic THP-1 cells to produce superoxide anion. Phorbol ester-stimulated superoxide generation and mRNA for gp91^<phox> in paralel with mRNAs for p47^<phox>, and p67^<phox> were significantly increased in E. chaffeensis-infected THP-1 cells. These increases were also achieved in THP-1 cells cultured in medium conditioned by the E. chaffeensis-infected cells, indicating that bystander cells can be activated for superoxide generation and implicating soluble factors in the response. Heat-stable and -unstable factors represented one-third and two-thirds of this activity, respectively. These results suggest that immature human monocytic cells increase their ability to generate superoxide anion in response to E. chaffeensis infection regardless they have been directly invaded or not. Further studies have suggested that these factors are exclusively derived from the bacteria.
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Research Products
(1 results)
