| Co-Investigator(Kenkyū-buntansha) |
SHIBATA Keisuke Saga Medical School, Internal Medicine, Research Associate, 医学部, 助手 (60244026)
MATSUZAKI Miwako Saga Medical School, Internal Medicine, Research Associate, 医学部, 助手 (80190445)
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| Research Abstract |
Legionella pneumophila, the agent that causes Legionnaires' disease, is a facultative intracellular bacterial pathogen that parasitizes human monocytes and alveolar macrophages. In compromised hosts, much attention has been paid to this bacterium. In this research, we studied on the infection of this intracellular bacterial pathogen in the differentiated leukemic cell lines and in monocytes from compromised hosts.
9-1. Cell lines and L.pneumophila infection
(1) We found intracellular multiplication of L.pneumophila in HL-60 cells functionally differentiated in responese to 1,25-dihydroxyvitamin D_3 and 22-oxacalcitriol (J.Leukoc.Biol.57,574-580,1995).
(2) We investigated the effects of interferon (IFN) alpha, beta, and gamma on the function of differentiated leukemic HL-60 cells induced by 1,25-dihydroxyvitamin D_3 (J.Interferon & Cytokine Res.16,347-356,1996).
9-2. Patients with adult T-cell leukemia/lymphoma (ATL) and human T-lymphotropic virus type I (HTLV-I) carriers as compromised hosts and their cytokine production
(1) We conducted ten-year survey of incidence of infection as a cause of death in hematologic malignancies, especially in ATL,by studying 90 autopsied cases (Acta Haematol.93,25-30,1995).
(2) We found increased production of interferon gamma but not interleukin 4 in HTLV-I carriers (Int J.Hematol.64,111-118,1996).
9-3. Host defense against L.pneumophila infection in HTLV-I carriers and patients with ATL
(1) We elucidated the differences in immune functions between HTLV-I carriers and patients with ATL (Clin.Immunol.Immunopathol.80,325-332,1996).
(2) We found marked inhibition of the intracellular multiplication of L.pneumophila in monocytes isolated from HTLV-I carriers. This was due to the increased production of IFN-gamma by CD4^+T-lymphocytes and of TNF-alpha (tumor necrosis factor alpha) by monocytes. Such inhibition was not observed in ATL patients and HTLV-I seronegative controls (J.Leukoc.Biol., in press, 1977).
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