Attempts to elucidate reasons why mycobacterial infections are intractable, by using an experimental mouse infection model
This paper reviews some recent studies which have been performed by us and other investigators, in order to clarify the reason why most mycobacterial infections such as due to Mycobacterium tuberculosisand M. avium complex infections are intractable, that is, why these organisms can escape from atta...
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| Published in | JAPANESE JOURNAL OF LEPROSY Vol. 65; no. 3; pp. 155 - 165 |
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| Main Author | |
| Format | Journal Article |
| Language | Japanese |
| Published |
Japan
Japanese Leprosy Association
1996
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1342-3681 1884-314X |
| DOI | 10.5025/hansen.65.155 |
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| Abstract | This paper reviews some recent studies which have been performed by us and other investigators, in order to clarify the reason why most mycobacterial infections such as due to Mycobacterium tuberculosisand M. avium complex infections are intractable, that is, why these organisms can escape from attack by microbicidal mechanisms of host macrophages and consequently persist for long time at sites of infection. This paper mainly dealt with the two major subjects, which were studied by using an experimental model for murine M. avium infection. The first subject is on the modes and mechanisms of mycobacterial killing in host macrophages and the mechanisms of bacterial escape from an onslaught by macrophages. The second is on the characteristics of immunosuppressive macrophages induced in M. avium complex infection and the role of the suppressor macrophages in the establishment of immune unresponsiveness of host mice in the progressed stage of infection. |
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| AbstractList | This paper reviews some recent studies which have been performed by us and other investigators, in order to clarify the reason why most mycobacterial infections such as due to Mycobacterium tuberculosis and M. avium complex infections are intractable, that is, why these organisms can escape from attack by microbicidal mechanisms of host macrophages and consequently persist for long time at sites of infection. This paper mainly dealt with the two major subjects, which were studied by using an experimental model for murine M. avium infection. The first subject is on the modes and mechanisms of mycobacterial killing in host macrophages and the mechanisms of bacterial escape from an onslaught by macrophages. The second is on the characteristics of immunosuppressive macrophages induced in M. avium complex infection and the role of the suppressor macrophages in the establishment of immune unresponsiveness of host mice in the progressed stage of infection. This paper reviews some recent studies which have been performed by us and other investigators, in order to clarify the reason why most mycobacterial infections such as due to Mycobacterium tuberculosis and M. avium complex infections are intractable, that is, why these organisms can escape from attack by microbicidal mechanisms of host macrophages and consequently persist for long time at sites of infection. This paper mainly dealt with the two major subjects, which were studied by using an experimental model for murine M. avium infection. The first subject is on the modes and mechanisms of mycobacterial killing in host macrophages and the mechanisms of bacterial escape from an onslaught by macrophages. The second is on the characteristics of immunosuppressive macrophages induced in M. avium complex infection and the role of the suppressor macrophages in the establishment of immune unresponsiveness of host mice in the progressed stage of infection.This paper reviews some recent studies which have been performed by us and other investigators, in order to clarify the reason why most mycobacterial infections such as due to Mycobacterium tuberculosis and M. avium complex infections are intractable, that is, why these organisms can escape from attack by microbicidal mechanisms of host macrophages and consequently persist for long time at sites of infection. This paper mainly dealt with the two major subjects, which were studied by using an experimental model for murine M. avium infection. The first subject is on the modes and mechanisms of mycobacterial killing in host macrophages and the mechanisms of bacterial escape from an onslaught by macrophages. The second is on the characteristics of immunosuppressive macrophages induced in M. avium complex infection and the role of the suppressor macrophages in the establishment of immune unresponsiveness of host mice in the progressed stage of infection. This paper reviews some recent studies which have been performed by us and other investigators, in order to clarify the reason why most mycobacterial infections such as due to Mycobacterium tuberculosisand M. avium complex infections are intractable, that is, why these organisms can escape from attack by microbicidal mechanisms of host macrophages and consequently persist for long time at sites of infection. This paper mainly dealt with the two major subjects, which were studied by using an experimental model for murine M. avium infection. The first subject is on the modes and mechanisms of mycobacterial killing in host macrophages and the mechanisms of bacterial escape from an onslaught by macrophages. The second is on the characteristics of immunosuppressive macrophages induced in M. avium complex infection and the role of the suppressor macrophages in the establishment of immune unresponsiveness of host mice in the progressed stage of infection. |
| Author | Tomioka, Haruaki |
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| References | 12) Kanai, K. and Kondo, K.: Antibacterial and cytoxic aspects of long chain fatty acids as cell surface events: selected topics. Jpn. J. Med. Sci. Biol. 32:135-174 (1979). 17) 冨岡治明:Mycobacterium intracellulare感染マウスに誘導される免疫抑制性マクロファーDジの性状.結核68:767-775(1993). 11) Tomioka, H. and Saito, H.: Macrophage chemiluminescence induced by interaction with transparent and opaquecolonial variants of Mycobacterium intracellulare. J. Gen. Microbiol. 139: 3011-3015 (1993). 18) Tomioka, H., Sato K., Maw, W. W., et al.: The role of tumor necrosis factor, interferon-γ, transforming growth factor-β, and nitric oxide in the expression of immunosuppressive functions of splenic macrophages induced by Mycobacterium avium complex infection. J. Leuk. Biol. 58:704-712 (1995). 2) Trinchieri, G.: Interleukin-12 and its role in the generation of TH-1 cells. Immunol. Today 14:335-337 (1993). 8) Chan, J. , Xing, Y., Magliozzo, R. S., et al.: Killing of virulent Mycobacterium tuberculosis by reactive nitrogen intermediates produced by activated murine macrophages. J. Exp. Med. 175: 1111-1122 (1992) . 9) Yamada, Y. , Saito, H. , Tomioka, Jpn. J. Leprosy 65, 155-165(1996) H., et al.: Susceptibility of microorgan-isms to active oxygen species: Sensitivity to the xanthine-oxidase-mediated antimicrobial system. J. Gen. Mi-crobiol. 133:2007-2014 (1987). 20) Tomioka, H., Kishimoto, T., and Maw, W. W.: Phospholipids and reactive nitrogen intermediates collaborate in expression of the T cell mitogenesis-inhibitory activity of immunosuppressive macrophages induced in mycobacterial infection. Clin. Exp. Immunol. 103:219-225(1996). 16) Tomioka, H , and Saito, H.: Characterization of immunosuppressive functions of murine peritoneal macrophages induced with various agents. J. Leuk. Biol. 51: 24-31 (1992). 13) Saito, H. and Tomioka, H.: Susceptibiltiy of transparent, opaque, and rough colonial variants of Mycobacteriumavium complex to various fatty acids. Antimicrob. Agents Chemother. 32:400-402 (1988) . 10) Yamada, Y., Saito, H., Tomioka, H., et al.: Relationship between the susceptibility of various bacteria to active oxygen species and to intracellulare killing by macrophages. J. Gen. Microbiol. 133:2015-2021(1987). 1) 冨岡治明:抗酸菌感染症が難治性である理由を探る.日本細菌学雑誌,50:687-701(1995). 19) Tomioka, H., Maw, W. W., Sato, K., et al.: The role of tumor necrosis factor-α in combination with interferon-γ or iriterleukin-1 in the induction of immunosuppressive macrophages due to Mycobacterium avium complex infection. Immunology 88:61-67 (1996). 4) Mosmann, T. R. and Moore, K. W.: The role of IL-10 in crossregulation of TH1 and TH2 responses. Immunol. Today 12:A49-53 (1991). 14) Tomioka, H., Saito, H., and Yamada, Y.: Characteristics of immunosuppressive macrophages induced in spleen cells by Mycobacterium avium complex infections in mice. J. Gen. Microbiol. 136:965-973 (1990). 15) Tomioka, H., Saito, H., and Sato, K.: Characterization of immunosuppressive macrophages induced in host spleen cells by Mycobacterium avium complex and Mycobacterium tuberculosis infections in mice. Microbiol. Immunol. 34:283-297, (1990). 6) Bermudez, L. E. and Champsi, J. A.: Infection with Mycobacterium avium induced production of interleukin-10 (IL-10), and administration of anti-IL-10 antibody is associated with enhanced resistance to infection in mice. Infect. Immun. 61:3093-3097 (1993). 3) Castro, A. G . , Silva , R. A. , and Appelberg, R.: Endogenously produced IL-12 is required for the induction of protective T cells during Mycobacterium avium infections in mice. J. Immunol. 155: 2013-2019 (1995). 5) Bermudez, L. E.: Production of transforming growth factor -β by Mycobacterium avium-infected human macrophagesis associated with unresponsiveness to IFN-γ . J. Immunol. 150:1838-1845 (1993). 7) Chan, J. and Kauf mann , H. E.: Immune mechanisms of protection. In: Tuberculosis. Pathogenesis, Protection,and Control. (ed by B. R. Bloom) p. 389-415, ASM Press, Washington, DC. (1994). |
| References_xml | – reference: 16) Tomioka, H , and Saito, H.: Characterization of immunosuppressive functions of murine peritoneal macrophages induced with various agents. J. Leuk. Biol. 51: 24-31 (1992). – reference: 2) Trinchieri, G.: Interleukin-12 and its role in the generation of TH-1 cells. Immunol. Today 14:335-337 (1993). – reference: 7) Chan, J. and Kauf mann , H. E.: Immune mechanisms of protection. In: Tuberculosis. Pathogenesis, Protection,and Control. (ed by B. R. Bloom) p. 389-415, ASM Press, Washington, DC. (1994). – reference: 20) Tomioka, H., Kishimoto, T., and Maw, W. W.: Phospholipids and reactive nitrogen intermediates collaborate in expression of the T cell mitogenesis-inhibitory activity of immunosuppressive macrophages induced in mycobacterial infection. Clin. Exp. Immunol. 103:219-225(1996). – reference: 10) Yamada, Y., Saito, H., Tomioka, H., et al.: Relationship between the susceptibility of various bacteria to active oxygen species and to intracellulare killing by macrophages. J. Gen. Microbiol. 133:2015-2021(1987). – reference: 15) Tomioka, H., Saito, H., and Sato, K.: Characterization of immunosuppressive macrophages induced in host spleen cells by Mycobacterium avium complex and Mycobacterium tuberculosis infections in mice. Microbiol. Immunol. 34:283-297, (1990). – reference: 5) Bermudez, L. E.: Production of transforming growth factor -β by Mycobacterium avium-infected human macrophagesis associated with unresponsiveness to IFN-γ . J. Immunol. 150:1838-1845 (1993). – reference: 8) Chan, J. , Xing, Y., Magliozzo, R. S., et al.: Killing of virulent Mycobacterium tuberculosis by reactive nitrogen intermediates produced by activated murine macrophages. J. Exp. Med. 175: 1111-1122 (1992) . – reference: 3) Castro, A. G . , Silva , R. A. , and Appelberg, R.: Endogenously produced IL-12 is required for the induction of protective T cells during Mycobacterium avium infections in mice. J. Immunol. 155: 2013-2019 (1995). – reference: 13) Saito, H. and Tomioka, H.: Susceptibiltiy of transparent, opaque, and rough colonial variants of Mycobacteriumavium complex to various fatty acids. Antimicrob. Agents Chemother. 32:400-402 (1988) . – reference: 18) Tomioka, H., Sato K., Maw, W. W., et al.: The role of tumor necrosis factor, interferon-γ, transforming growth factor-β, and nitric oxide in the expression of immunosuppressive functions of splenic macrophages induced by Mycobacterium avium complex infection. J. Leuk. Biol. 58:704-712 (1995). – reference: 4) Mosmann, T. R. and Moore, K. W.: The role of IL-10 in crossregulation of TH1 and TH2 responses. Immunol. Today 12:A49-53 (1991). – reference: 6) Bermudez, L. E. and Champsi, J. A.: Infection with Mycobacterium avium induced production of interleukin-10 (IL-10), and administration of anti-IL-10 antibody is associated with enhanced resistance to infection in mice. Infect. Immun. 61:3093-3097 (1993). – reference: 19) Tomioka, H., Maw, W. W., Sato, K., et al.: The role of tumor necrosis factor-α in combination with interferon-γ or iriterleukin-1 in the induction of immunosuppressive macrophages due to Mycobacterium avium complex infection. Immunology 88:61-67 (1996). – reference: 9) Yamada, Y. , Saito, H. , Tomioka, Jpn. J. Leprosy 65, 155-165(1996) H., et al.: Susceptibility of microorgan-isms to active oxygen species: Sensitivity to the xanthine-oxidase-mediated antimicrobial system. J. Gen. Mi-crobiol. 133:2007-2014 (1987). – reference: 1) 冨岡治明:抗酸菌感染症が難治性である理由を探る.日本細菌学雑誌,50:687-701(1995). – reference: 12) Kanai, K. and Kondo, K.: Antibacterial and cytoxic aspects of long chain fatty acids as cell surface events: selected topics. Jpn. J. Med. Sci. Biol. 32:135-174 (1979). – reference: 11) Tomioka, H. and Saito, H.: Macrophage chemiluminescence induced by interaction with transparent and opaquecolonial variants of Mycobacterium intracellulare. J. Gen. Microbiol. 139: 3011-3015 (1993). – reference: 17) 冨岡治明:Mycobacterium intracellulare感染マウスに誘導される免疫抑制性マクロファーDジの性状.結核68:767-775(1993). – reference: 14) Tomioka, H., Saito, H., and Yamada, Y.: Characteristics of immunosuppressive macrophages induced in spleen cells by Mycobacterium avium complex infections in mice. J. Gen. Microbiol. 136:965-973 (1990). |
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| SubjectTerms | Animals Bactericidal mechanisms Cytokines - physiology Disease Models, Animal Humans Immunosuppressive macrophages M. avium complex Macrophages Macrophages - immunology Mice Mycobacteria Mycobacterium avium Complex - pathogenicity Mycobacterium avium-intracellulare Infection - immunology Mycobacterium avium-intracellulare Infection - microbiology Mycobacterium tuberculosis - pathogenicity Phagocytosis Tuberculosis - immunology Tuberculosis - microbiology |
| Title | Attempts to elucidate reasons why mycobacterial infections are intractable, by using an experimental mouse infection model |
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