1994 Fiscal Year Final Research Report Summary
Escape mechanisms of intracellular bacteria and the analysis of protective immunity and tissue damage in the infected host
| Project/Area Number |
05454190
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Bacteriology (including Mycology)
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| Research Institution | Niigata University |
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Principal Investigator |
MITSUYAMA Masao Niigata University School of Medicine, Professor, 医学部, 教授 (10117260)
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| Co-Investigator(Kenkyū-buntansha) |
KAWAMURA Ikuo Niigata University School of Medicine, Assistant Professor, 医学部, 助手 (20214695)
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| Project Period (FY) |
1993 – 1994
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| Keywords | intracellular bacteria / protective immunity / tissue damage / Listeria monocytogenes / Mycobacterium / cytokine / virulence factor / escape mechanism |
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| Research Abstract |
One of the purpose of this study was to study the escape mechanisms of intracellular bacteria and its contribution to the induction of cell-mediated immunity (CMI) in infected hosts. In addition, we wanted to segregate the protective T cells and those involved in tissue damage with respect to T cell function and antigen in recognition. The following results were obtained in the experiments using murine models of infection.
1. LLO (listeriolysin O) encoded by hlya plays a crucial role in the escape of Listeria monocytogenes. LLO is capable of inducing various cytokines in macrophages in addition to its primary effect on cell membrane. 2. Only those strain of Listeria capable of expressing hlya induce CMI.LLO appeared to induce the functional development of T cells through its ability to induce IL-1alpha and IFN-gamma in the host. 3. Protective immunity is exerted by Th1 type CD4^+ T cells by producing a qreat amout of IFN-gamma in an antigen-specific manner. CD4^+ T cells with poor ability to produce IFN-gamma were only active in expression of delayd-type hypersensitivity. 4. Protective T cells recognize a wide range of antigens in L.monocytogenes, while BCG-reactive IFN-gamma-producing CD4^+ T cells recognize mainly 18 to 20kDa antigen. Peripheral blood lymphocytes from tuberculous patients showed a good response against this particular antigen resulting in IFN-gamma production. 5. CD8^+ T cells generated in L.monocytogenes-infected host seemed to contribute to tissue damage through production of TNF.6. Among various cytokines which are non-specifically produced in infected host, NK cell-derived IFN-gamma was critically important in the expression of iNOS (inducible NOS) and was unique to viable bacterial infection.
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