| Project/Area Number |
13670606
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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 |
Respiratory organ internal medicine
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| Research Institution | OITA MEDICAL UNIVERSITY |
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Principal Investigator |
NAGAI Hiroyuki Oita Medical University, Department of Medicine, Assistant Professor, 医学部, 助手 (80237487)
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| Co-Investigator(Kenkyū-buntansha) |
NASU Masaru Oita Medical University, Department of Medicine, Professor, 医学部, 教授 (70039874)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2002: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2001: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Deep seated mycosis / Trichosporon asahii / PCR (polymerase chain reaction) method / GXM (gluculoxylomannan) antigen / (1→3)-β-D glucan / environmental isolates / clinical isolates / gluculonoxylomannan抗原 / (1→3)β-D glucan / Trichosporon ashahii |
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| Research Abstract |
(1) Trichosporon asahii (T. asahii) is one of a number of opportunistic mycotic pathogens that can cause life-threatening infections in immunocompromised patients. Several investigators have reported that gluculonoxylomannan (GXM) antigens of clinical isolates are higher than that of environmental isolates. Other reports, clinical important fungi such as Candida albicans and Cryptococcus neoformans are known to change their phenotype after repeated subculture or in-vivo passages, and this process is thought to allow some fungi to escape eradication by the host immune system. However there are no studies for morphological changes of Trichosporon asahii after passages in vivo. This study investigated whether in-vivo passages of environmental isolates of Trichosporon asahii in mice changes their phenotype and pathogenicity.
(2) The shape of colonies and cell types were clearly different in environmental and clinical isolates. Furthermore, the clinical isolates released significantly higher levels of GXM antigen than environmental isolates. The phenotype of passaged isolates was significantly different from the original environmental isolates with respect to the morphology of colonies and cell type and GXM release. In vivo, toxicity of the environmental isolates was higher than clinical isolates and passaged isolates.
(3) These results suggest that the phenotypic changes in T. asahii occur as a result of in-vivo passages. This process may allow a proportion of the fungal population to escape eradication by the host immune system, as GXM antigen is considered to protect the fungi against phagocytosis by polymorphonuclear leucocytes and monocytes in vivo.
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