Phagocytosis of <i>Mycobacterium</i> <i>leprae</i> down-regulates anti-microbial activity of murine macrophages against <i>Mycobacterium intracellulare</i>
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- TATANO Yutaka
- Department of Microbiology and Immunology, Shimane University School of Medicine
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- SANO Chiaki
- Department of Microbiology and Immunology, Shimane University School of Medicine
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- EMORI Masako
- Department of Microbiology and Immunology, Shimane University School of Medicine
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- SAITO Hajime
- Department of Microbiology and Immunology, Shimane University School of Medicine
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- SATO Katsumasa
- Department of Microbiology and Immunology, Shimane University School of Medicine
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- SHIMIZU Toshiaki
- Department of Microbiology and Immunology, Shimane University School of Medicine
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- TOMIOKA Haruaki
- Department of Microbiology and Immunology, Shimane University School of Medicine
Bibliographic Information
- Other Title
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- らい菌貪食に伴うマクロファージの抗<i>Mycobacterium intracellulare</i> 殺菌能の低下
- Phagocytosis of Mycobacterium leprae down-regulates anti-microbial activity of murine macrophages against Mycobacterium intracellulare
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Abstract
Patients with highly bacillated lepromatous leprosy (LL) essentially lack T cell-mediated immune responses specific to Mycobacterium leprae (ML) antigens, resulting in severely impaired host resistance to leprosy bacilli. Such type of immune unresponsiveness characteristic of LL patients is mainly attributable to markedly depressed T cell ability to activate/expand in response to ML antigens. In this study, we examined profiles of antimycobacterial activity of macrophages, which phagocytized leprosy bacilli, because there is another possibility that, in LL patients, host macrophages in the leprosy lesions are impaired in their antimicrobial activity due to their interaction with infected leprosy bacilli, particularly cellular events through binding with and/or internalization of the pathogens, thereby causing the reduction in host resistance to ML pathogens. The present study indicated the following. First, the anti-M. avium complex activity of murine peritoneal macrophages was significantly reduced when they had phagocytosed heat-killed leprosy bacilli. Second, infection of macrophages with leprosy bacilli did not affect macrophage-mediated suppressor activity against T cell proliferative response to Concanavalin A. These findings indicate that macrophage's intracellular signaling pathways that are up-regulated in response to phagocytosis of leprosy bacilli are linked to the signaling cascades participating in macrophage antimicrobial functions, but not cross-talk with those allowing the expression of macrophage's suppressor activity against T cell functions.
Journal
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- JAPANESE JOURNAL OF LEPROSY
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JAPANESE JOURNAL OF LEPROSY 81 (3), 175-183, 2012
Japanese Leprosy Association
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Keywords
Details 詳細情報について
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- CRID
- 1390001206322843776
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- NII Article ID
- 10031026287
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- NII Book ID
- AN10559906
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- COI
- 1:STN:280:DC%2BC3s%2Fgt1yjsQ%3D%3D
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- ISSN
- 1884314X
- 13423681
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- PubMed
- 23012845
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- Text Lang
- ja
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- Data Source
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- JaLC
- Crossref
- PubMed
- CiNii Articles
- KAKEN
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- Abstract License Flag
- Disallowed