| Co-Investigator(Kenkyū-buntansha) |
KAWAKAMI Kazuyoshi University of the Ryukyus, Faculty of Medicine, Assistant, 医学部, 助手 (10253973)
KANESHIMA Hiroshi University of the Ryukyus, Faculty of Medicine, Assistant, 医学部, 助手 (00185943)
普久原 浩 琉球大学, 医学部, 助手 (10218951)
中村 浩明 琉球大学, 医学部, 助手 (10189053)
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| Budget Amount *help |
¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1994: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1993: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Research Abstract |
In this study, HTLV-I-positive and negative patients with chronic bronchial diseases were clinically analyzed in Okinawa prefecture, one of the endemic areas of infection with this virus. Nosignificant difference was found between these two groups in the following clinical parameters : smoking, HLA-Bw54, chronic parasinusitis, titer of cold hemagglutinin, causative microorganisms in acute exacerbation, FEV1.0, arterial blood oxygen pressure. In immunological parameters, PPD skin test, proportion of CD3 positive cells and CD4/CD8 ratio in peripheral blood mononuclear cells (PBMC), and serum level of soluble IL-2 receptor (sIL-2R) did not show any significant differences, while spontaneous proliferation of PBMC was more frequently observed in HTLV-I positive patients than in negative ones. In addition, in virus negative group, serum sIL-2R level showed a tendency to decrease after long tretment with macrolide antibiotics, while in virus positive group, such finding was not observed.
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T cell lines infected with HTLV-I were established from the bronchoalveolar (BAL) fluid cells of virus carriers. These T cells lost CD3/antigen receptor complex on their surface earlier than T cell lines established from PBMC of the same patients during in vitro culture. In addition, production of IL-2 by BAL T cells stimulated via antigen receptor was reduced concomitantly with its disappearance. These T cells spontaneously produced much amount of IL-6 and TNF-alpha, raising a possibility of their involvement in the pathogenesis of lung disorders caused by HTLV-i infection. Therefore, we tried to establish an animal model of HAB by intratracheal injection of these T cells into SCID mice. In this trial, however, the inoculated cells rapidly disappeared from the lungs, 4 weeks later the viral DNA was not detected by PCR method, and we failed to establish mice persistently infected with HTLV-I.In histological examination, no apparent finding was observed in their lungs. Thus, the HAB model failed to be established in this study. Less
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