1996 Fiscal Year Final Research Report Summary
Mechanism of development of diarrhea by enteric bacteria
| Project/Area Number |
08407011
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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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 | Research Institute, International Medical Center of Japan |
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Principal Investigator |
TAKEDA Yoshifumi International Medical Center of Japan, Research Institute, Directou-general, 研究所, 所長 (30029772)
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| Co-Investigator(Kenkyū-buntansha) |
HAMABATA Takashi International Medical Center of Japan, Research Institute, Division Chief, 研究所, 室長 (40311427)
YAMASAKI Shinji International Medical Center of Japan, Research Institute, Division Chief, 研究所, 室長 (70221653)
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| Project Period (FY) |
1996 – 1998
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| Keywords | Vibrio cholerae / Shigella dysenteriae / enterohemorrhagic E.coli / cholera enterotoxin / Aquaporin / Shiga toxin gene / O157 antigen synthesisi gene / IL-8 induction |
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| Research Abstract |
(1) Mechanism of diarrheagenicity of Vibrio choleras.
(1)Gienes for aquaporin (AQP)1, AQP3 and AQP4 were cloned and expressed in Xenopus oocytes. Cholera enterotoxin stimulated water permeability by. AQP4 but inhitied the effect of AQP3.
(2)RA mutant cholera enterotoxin A subunit (S61F) that has no ADP-ribosyltransferase activity lost its diarrheagenicity but retained- its adjuvant activity. The S61F elicited Th-2 type mucosal immunity.
(3)A mutant cholera enterotoxin B subunit (E11R) lost its biological activity.
(4)Anon-membrance-damaging cytotoxin was isolated from non-O1 Vibrio cholerae.
(2) Mechanism of diarrheagenicity of Shigella dysenteriae. Diarrheal activity of a cytolethal distending toxin isolated from Shigella dysenteriae was demonstrated in suckling mice.
(3) Mechanism of diarrheagenicity of enterohemorrhagic Escherichia coli.
(1)Lysogenic phages that carry a new Shiga toxin gene was isolated from enterohemorrhagic E. coli.
(2)Genes responsible for O157 antigen synthesis were identified.
(3)Induction of IL-8 in CaC0-2 cells by Stx-1 and St-2 was demonstrated. The activity of the toxins required RNA N-glycosidase.
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