2000 Fiscal Year Final Research Report Summary
A STUDY OF TYPE II ALVEOLAR EPITHELIAL CELLS AS INFECTION SITE OF ACID-FAST BACILLI
| Project/Area Number |
10670545
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | SHIMANE MEDICAL UNIVERSITY |
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Principal Investigator |
SATO Katsumasa SHIMANE MEDICAL UNIVERSITY, MICROBIOLOGY AND IMMUNOLOGY, INSTRUCTOR, 医学部, 助手 (00142331)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMIZU Toshiaki SHIMANE MEDICAL UNIVERSITY, MICROBIOLOGY AND IMMUNOLOGY, INSTRUCTOR, 医学部, 助手 (60284030)
TOMIOKA Haruaki SHIMANE MEDICAL UNIVERSITY, MICROBIOLOGY AND IMMUNOLOGY, PROFESSOR, 医学部, 教授 (40034045)
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| Project Period (FY) |
1998 – 2000
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| Keywords | ACID-FAST BACIL II / MYCOBACTERIUM TUBERCULOSIS / MYCOBACTERIUM AVIUM COMPLEX / TYPE II ALVEOLAR EPITHELIAL CELLS / MACROPHAGES / A-549 CELLS / INVASION / CYTOKINES |
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| Research Abstract |
1. Antimicrobial effects of clarithromycin (CAM), KRM-1648 (KRM) and levofloxacin (LVFX) against Mycobacterium tuberculosis (MTB) or M.avium complex (MAC) residing in the A-549 human type II alveolar epithelial cells (A-549 cells) were less than the effects of the same drugs against the same organisms residing in Mono Mac 6 human macrophage-like cells (MM6-MΦ).
2. Antimicrobial activities of these drugs against MTB and MAC adapted to an intramacrophagic environment (intracellularly adapted : I-type) and those passaged in the 7H9 liquid medium (extracellularly adapted : E-type) were studied. The antibacterial effect of CAM or LVFX against E-type MTB or MAC residing in MM6-MΦs or A-549 cells was stronerg than a case against I-type MTB or MAC within the same cells. On the other hand, the antibacterial effect of KRM for E-type MTB or MAC residing in both cells was weaker than a case for I-type organisms within the same cells.
3. Mice were infected intratracheally with MTB or MAC, and the lung sections of the infected mice were observed with transmission electron photomicrographs. The infected bacteria were recognized in type II alveolar epithelial cells in addition to mature granulocytes and macrophages.
4. Using a dual chamber system, we examined whether the humoral factor of the A-549 cells infected with MTB or MAC which were released, influenced the anti-MTB or the anti-MAC antibacterial activity of MM6-MΦs. The number of the MTB or MAC organisms residing in MM6-MΦs of the top-chamber was decreased by the existence of A-549 cells infected with the MTB or MAC.
5. It was found that the humoral factor (s) that decreased the number of these bacteria might be TNF-α and/or GM-CSF with RT-PCR examination.
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