2003 Fiscal Year Final Research Report Summary
Study on molecular basis of bacteria-host cell interaction in enteropathogenic Escherichia coli adherence.
| Project/Area Number |
14570236
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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 | Osaka University |
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Principal Investigator |
TOBE Toru Osaka University Graduate School of Medicine, Associate Professor, 医学系研究科, 助教授 (70207596)
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| Project Period (FY) |
2002 – 2003
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| Keywords | adhernce / pathogenicity / TTSS / transcriptional regulation / pathogenic E.coli / III型分泌 |
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| Research Abstract |
Enteropathogenic Escherichia coli is a causative agent of diarrhea in human. Adherence to intestinal epithelial cells is crucial for EPEC pathogenicity. Expression of adherence factors and type III secretion activity have shown to be altered during #4 adhesion to epithelial cells. By using DNA microarray, we determined transcript levels of plasmid-or chromosome-oriented virulence-associated genes as well as other EAF plasmid-coding genes in EPEC during adherent to Caco-2 cells. Transcriptions of genes in bfp operon, LEE4 (esp) operon and LEE5 (tir-eae) Operon were enhanced within 1 h after infection, although transcriptions of genes encoding type Ill machinery were not enhanced. Tran8script levels of bfp genes decreased at 2 h post-infection, while transcript levels of LEE4 and LEE5 operon stayed at high for 4-5 h and then decreased at later stage of adherence (5-6 h post infection). On the other hand, transcription of genes presumed to be involved in replication of EAF plasmid increased remarkably at later stage. The copy number of EAF plasmid against chromosome increased at later stage. Enhancement of bfp, LEE4 or LEE5 transcription was not abolished by escC mutation or eae mutation, while, reduction of LEE4 and LEE5 transcription at later stage and increase of EAF plasmid copy number was diminished by these mutations. The results suggested that transcription of bfp~, LEE4 and LEE5 operons were enhanced or repressed differentially during adherence by responding to changes in interaction with host cells.
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