Combined Program on Microbiology and Immunology. Osaka University.

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Research Theme :
Analysis of the pathogenesis and control of enterobacterial infection

Principal Research Scientist
Takeshi Honda
Profile:

[Research/Education]

Mar. 1970, Graduated from Osaka University, School of Medicine, Internship in Internal Medicine (1970 – 1973)
1973, Research Associate, Research Institute of Microbial Disease, Osaka University
[Project] Vibrio parahaemolyticus TDH (toxin)
1977 –1979, Visiting researcher at the University of Texas
[Project] Vibrio cholerae vaccine
1979, Research Associate, Research Institute of Microbial Disease, Osaka University
[Project] Enteropathogenic Escherichia coli (in particular, ETEC)
1984, Associate Professor, Research Institute of Microbial Disease, Osaka University
[Project] Enteropathogenic Escherichia coli (in particular, EHEC)
1991, Professor, Research Institute of Microbial Disease, Osaka University
[Project] Continuation/extension of previous research objectives and pursuit of a new field in Genome analysis, Molecular Biology, Electrophysiology, Microbiology, and etc.

[Positions]

Osaka University:
Bacteriology, School of Medicine(4 units), Bacteriology, School of Dentistry(2 units),
School of Pharmaceutical Science (3 units), Graduate School of Pharmaceutical Science (Pathogenic Microbiology, 15 units), School of Engineering (Food Microbiology, 5 units)
Other organizations:
Part-time lecturer at Osaka Medical College, Institute of Tropical Medicine, Nagasaki University, Aichi Medical University, The Institute of Medical Science, The University of Tokyo, Okayama University, Medical School, Kyoto Prefecture University of Medicine,
Faculty on Kyoto University, School of Medicine, and Kobe University, School of Medicine, and etc.

[Awards]

Kuroya Award from Japanese Society for Bacteriology (1977)
Futaki Award from Japanese Association for Infectious Diseases (1991)
Kojima Saburou Memorial Award from Kurozumi Medical Foundation (1997)
Asakawa Award from Japanese Society for Bacteriology (2003)

Collaborators

Tetsuya Iida, Toshio Kodama, Post-doctoral fellows (2), Graduate students (4)

Vlademir Vicente Cantarelli (Research Associate of COE)

Research Summary

Enterobacterial infection (diarrhea) is a major social concern especially in the developing world, and still claims the lives of 300 million people per year. Therefore, establishing countermeasures against enterobacterial infection remains an urgent and important matter. Using three species of bacteria, enteropathogenic Escherichia coli, Vibrio parahaemolyticus, and Providencia, which each possess a unique mechanism of infection, as models of enterobacterial infection, we aim to: 1) identify the pathogenic factor relevant to each infectious disease, 2) analyze the responsive mechanisms of host cells against infection, 3) investigate the similarities and differences in pathogenesis of these three species of bacteria, 4) further understand the process of bacterial infection of the intestine, and finally 5) find clues which will help in the development of novel countermeasures against enterobacterial infection based on the information obtained from our research projects. In this project, we mainly compare the mechanisms of microbial attachment to host cells. Attachment occurs at the initial stage of infection, and comprises three different mechanisms (simple attachment, attachment and formation of A/E (attaching and effacing) lesions, and entry into the target cells). We also compare the biological responses of the host cells, in order to clarify the characteristics of each bacterium and the pathogenic processes common among these bacteria. Further understanding of the mechanism of each enterobacterial infection (especially pathogenic Providencia-induced diarrhea, which we recently discovered) will provide valuable information regarding the treatment of each infection, will help establish new prophylactic treatments, and will promote public health improvement. We believe that we have a tremendous amount of accumulated know-how in the research of enterobacterial infection, and that we have a great advantage because we are studying three species which possess (or at least are thought to have) different pathogenic mechanisms within the same laboratory. In particular, our recent study demonstrated that these three species share a common pathogenic process, which induces pathogenic changes (lesions) in target cells through a type III secretion system (TTSS). Now we seek to investigate the mechanisms of infection based on this newly discovered process.

Publications

1. Hayashi T, K. Makino, M. Ohnishi, K. Kurokawa, K. Ishii, K. Yokoyama, C. G. Han,
E. Ohtsubo, K.Nakayama, T.Murata, M.Tanaka, T.Tobe, T.Iida, H.Takami, T.Honda, C.Sasakawa,N.Ogasawara, T. Yasunaga, S. Kuhara, T. Shiba, M. Hattori and H. Shinagawa: Complete genome sequence of enterohemorrhagic Escherichia coli O157:H7 and genomic comparison with a laboratory strain K-12. DNA Research. 8:11-22, 2001

2. Murata T., T. Iida, Y. Shiomi, K. Tagomori, Y. Akeda, I. Yanagihara, S. Mushiake, F.
Ishiguro and T. Honda: A large outbreak of foodborne infection attributed to Providencia
alcalifaciens. J. Infect. Dis. 184: 1050-1055, 2001

3. Vlademir V. C, A. Takahashi, I. Yanagihara, Y. Akeda, K. Imura, T. Kodama, G. Kono,
Y. Sato and T. Honda: Talin, a host cell protein, interacts directly with the translocated
intimin receptor, Tir, of entropathogenic Escherichia coli, and is essential for pedestal
formation. Cellular Microbiology 3:1-8, 2001

4. Vlademir V. C., A. Takahashi, I. Yanagihara, Y. Akeda, K. Imura, T. Kodama, G. Kono,
Y. Sato, T. Iida and T. Honda : Cortactin necessary for F-actin accumulation in pedestal
structures induced by enteropathogenic Escherichia coli infection. Infect. Immun. 70:
2206-2209, 2002.

5. Makino K., K. Oshima, K. kurokawa, K. Yokoyama, T. Uda, K. Tagomori, Y.Iijima, M.
Najima, M. Nakano, A. Yamashita, Y. Kubota, S. Kimura, T. Yasunaga,T.Honda, H.
Shinagawa, M. Hattori, T. Iida: Genome sequence of Vibrio parahaemolyticus: a
pathogenic mechanism distinct from that of V. cholerae. Lancet 361: 743-749, 2003.