The stress-responsive chaperone α-crystallin 2 is required for pathogenesis of Mycobacterium tuberculosis
Mycobacterium tuberculosis has two members of the α-crystallin (Acr) family of molecular chaperones. Expression of Acr1 is induced by exposure to hypoxia or nitric oxide and is associated with bacterial persistence in a non-replicating state. Expression of Acr2 is induced by heat shock, oxidative st...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Stewart, Graham R. [verfasserIn] Newton, Sandra M. [verfasserIn] Wilkinson, Katalin A. [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2005 |
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| Umfang: |
Online-Ressource |
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2004 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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In: Molecular microbiology - Oxford [u.a.] : Wiley-Blackwell, 1987, 55(2005), 4, Seite 0 |
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volume:55 ; year:2005 ; number:4 ; pages:0 |
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10.1111/j.1365-2958.2004.04450.x |
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| 520 | |a Mycobacterium tuberculosis has two members of the α-crystallin (Acr) family of molecular chaperones. Expression of Acr1 is induced by exposure to hypoxia or nitric oxide and is associated with bacterial persistence in a non-replicating state. Expression of Acr2 is induced by heat shock, oxidative stress, and uptake by macrophages. We have shown that Acr2 continues to be expressed at a high level during both acute and chronic infection in the mouse model, with an increased ratio of acr2:acr1 mRNA in the persistent phase. Deletion of the acr2 gene resulted in a decrease in the resistance of M. tuberculosis to oxidative stress but did not impair growth in mouse bone marrow macrophages. There was no difference in bacterial load in mice infected with an acr2 deletion mutant, but a marked alteration in disease progression was evident from reduced weight loss over a prolonged infection. This correlated with reduced recruitment of T-cells and macrophages to the lungs of mice infected with the acr2 mutant and reduced immune-related pathology. These findings demonstrate that both α-crystallins contribute to persistent infection with M. tuberculosis and suggest that manipulation of acr expression can influence the host response to infection. | ||
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10.1111/j.1365-2958.2004.04450.x doi (DE-627)NLEJ24354250X DE-627 ger DE-627 rakwb Stewart, Graham R. verfasserin aut The stress-responsive chaperone α-crystallin 2 is required for pathogenesis of Mycobacterium tuberculosis Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mycobacterium tuberculosis has two members of the α-crystallin (Acr) family of molecular chaperones. Expression of Acr1 is induced by exposure to hypoxia or nitric oxide and is associated with bacterial persistence in a non-replicating state. Expression of Acr2 is induced by heat shock, oxidative stress, and uptake by macrophages. We have shown that Acr2 continues to be expressed at a high level during both acute and chronic infection in the mouse model, with an increased ratio of acr2:acr1 mRNA in the persistent phase. Deletion of the acr2 gene resulted in a decrease in the resistance of M. tuberculosis to oxidative stress but did not impair growth in mouse bone marrow macrophages. There was no difference in bacterial load in mice infected with an acr2 deletion mutant, but a marked alteration in disease progression was evident from reduced weight loss over a prolonged infection. This correlated with reduced recruitment of T-cells and macrophages to the lungs of mice infected with the acr2 mutant and reduced immune-related pathology. These findings demonstrate that both α-crystallins contribute to persistent infection with M. tuberculosis and suggest that manipulation of acr expression can influence the host response to infection. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| Newton, Sandra M. verfasserin aut Wilkinson, Katalin A. verfasserin aut Humphreys, Ian R. oth Murphy, Helen N. oth Robertson, Brian D. oth Wilkinson, Robert J. oth Young, Douglas B. oth In Molecular microbiology Oxford [u.a.] : Wiley-Blackwell, 1987 55(2005), 4, Seite 0 Online-Ressource (DE-627)NLEJ243926537 (DE-600)1501537-3 1365-2958 nnns volume:55 year:2005 number:4 pages:0 http://dx.doi.org/10.1111/j.1365-2958.2004.04450.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 55 2005 4 0 |
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10.1111/j.1365-2958.2004.04450.x doi (DE-627)NLEJ24354250X DE-627 ger DE-627 rakwb Stewart, Graham R. verfasserin aut The stress-responsive chaperone α-crystallin 2 is required for pathogenesis of Mycobacterium tuberculosis Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mycobacterium tuberculosis has two members of the α-crystallin (Acr) family of molecular chaperones. Expression of Acr1 is induced by exposure to hypoxia or nitric oxide and is associated with bacterial persistence in a non-replicating state. Expression of Acr2 is induced by heat shock, oxidative stress, and uptake by macrophages. We have shown that Acr2 continues to be expressed at a high level during both acute and chronic infection in the mouse model, with an increased ratio of acr2:acr1 mRNA in the persistent phase. Deletion of the acr2 gene resulted in a decrease in the resistance of M. tuberculosis to oxidative stress but did not impair growth in mouse bone marrow macrophages. There was no difference in bacterial load in mice infected with an acr2 deletion mutant, but a marked alteration in disease progression was evident from reduced weight loss over a prolonged infection. This correlated with reduced recruitment of T-cells and macrophages to the lungs of mice infected with the acr2 mutant and reduced immune-related pathology. These findings demonstrate that both α-crystallins contribute to persistent infection with M. tuberculosis and suggest that manipulation of acr expression can influence the host response to infection. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| Newton, Sandra M. verfasserin aut Wilkinson, Katalin A. verfasserin aut Humphreys, Ian R. oth Murphy, Helen N. oth Robertson, Brian D. oth Wilkinson, Robert J. oth Young, Douglas B. oth In Molecular microbiology Oxford [u.a.] : Wiley-Blackwell, 1987 55(2005), 4, Seite 0 Online-Ressource (DE-627)NLEJ243926537 (DE-600)1501537-3 1365-2958 nnns volume:55 year:2005 number:4 pages:0 http://dx.doi.org/10.1111/j.1365-2958.2004.04450.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 55 2005 4 0 |
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10.1111/j.1365-2958.2004.04450.x doi (DE-627)NLEJ24354250X DE-627 ger DE-627 rakwb Stewart, Graham R. verfasserin aut The stress-responsive chaperone α-crystallin 2 is required for pathogenesis of Mycobacterium tuberculosis Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mycobacterium tuberculosis has two members of the α-crystallin (Acr) family of molecular chaperones. Expression of Acr1 is induced by exposure to hypoxia or nitric oxide and is associated with bacterial persistence in a non-replicating state. Expression of Acr2 is induced by heat shock, oxidative stress, and uptake by macrophages. We have shown that Acr2 continues to be expressed at a high level during both acute and chronic infection in the mouse model, with an increased ratio of acr2:acr1 mRNA in the persistent phase. Deletion of the acr2 gene resulted in a decrease in the resistance of M. tuberculosis to oxidative stress but did not impair growth in mouse bone marrow macrophages. There was no difference in bacterial load in mice infected with an acr2 deletion mutant, but a marked alteration in disease progression was evident from reduced weight loss over a prolonged infection. This correlated with reduced recruitment of T-cells and macrophages to the lungs of mice infected with the acr2 mutant and reduced immune-related pathology. These findings demonstrate that both α-crystallins contribute to persistent infection with M. tuberculosis and suggest that manipulation of acr expression can influence the host response to infection. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| Newton, Sandra M. verfasserin aut Wilkinson, Katalin A. verfasserin aut Humphreys, Ian R. oth Murphy, Helen N. oth Robertson, Brian D. oth Wilkinson, Robert J. oth Young, Douglas B. oth In Molecular microbiology Oxford [u.a.] : Wiley-Blackwell, 1987 55(2005), 4, Seite 0 Online-Ressource (DE-627)NLEJ243926537 (DE-600)1501537-3 1365-2958 nnns volume:55 year:2005 number:4 pages:0 http://dx.doi.org/10.1111/j.1365-2958.2004.04450.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 55 2005 4 0 |
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10.1111/j.1365-2958.2004.04450.x doi (DE-627)NLEJ24354250X DE-627 ger DE-627 rakwb Stewart, Graham R. verfasserin aut The stress-responsive chaperone α-crystallin 2 is required for pathogenesis of Mycobacterium tuberculosis Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mycobacterium tuberculosis has two members of the α-crystallin (Acr) family of molecular chaperones. Expression of Acr1 is induced by exposure to hypoxia or nitric oxide and is associated with bacterial persistence in a non-replicating state. Expression of Acr2 is induced by heat shock, oxidative stress, and uptake by macrophages. We have shown that Acr2 continues to be expressed at a high level during both acute and chronic infection in the mouse model, with an increased ratio of acr2:acr1 mRNA in the persistent phase. Deletion of the acr2 gene resulted in a decrease in the resistance of M. tuberculosis to oxidative stress but did not impair growth in mouse bone marrow macrophages. There was no difference in bacterial load in mice infected with an acr2 deletion mutant, but a marked alteration in disease progression was evident from reduced weight loss over a prolonged infection. This correlated with reduced recruitment of T-cells and macrophages to the lungs of mice infected with the acr2 mutant and reduced immune-related pathology. These findings demonstrate that both α-crystallins contribute to persistent infection with M. tuberculosis and suggest that manipulation of acr expression can influence the host response to infection. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| Newton, Sandra M. verfasserin aut Wilkinson, Katalin A. verfasserin aut Humphreys, Ian R. oth Murphy, Helen N. oth Robertson, Brian D. oth Wilkinson, Robert J. oth Young, Douglas B. oth In Molecular microbiology Oxford [u.a.] : Wiley-Blackwell, 1987 55(2005), 4, Seite 0 Online-Ressource (DE-627)NLEJ243926537 (DE-600)1501537-3 1365-2958 nnns volume:55 year:2005 number:4 pages:0 http://dx.doi.org/10.1111/j.1365-2958.2004.04450.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 55 2005 4 0 |
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10.1111/j.1365-2958.2004.04450.x doi (DE-627)NLEJ24354250X DE-627 ger DE-627 rakwb Stewart, Graham R. verfasserin aut The stress-responsive chaperone α-crystallin 2 is required for pathogenesis of Mycobacterium tuberculosis Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Mycobacterium tuberculosis has two members of the α-crystallin (Acr) family of molecular chaperones. Expression of Acr1 is induced by exposure to hypoxia or nitric oxide and is associated with bacterial persistence in a non-replicating state. Expression of Acr2 is induced by heat shock, oxidative stress, and uptake by macrophages. We have shown that Acr2 continues to be expressed at a high level during both acute and chronic infection in the mouse model, with an increased ratio of acr2:acr1 mRNA in the persistent phase. Deletion of the acr2 gene resulted in a decrease in the resistance of M. tuberculosis to oxidative stress but did not impair growth in mouse bone marrow macrophages. There was no difference in bacterial load in mice infected with an acr2 deletion mutant, but a marked alteration in disease progression was evident from reduced weight loss over a prolonged infection. This correlated with reduced recruitment of T-cells and macrophages to the lungs of mice infected with the acr2 mutant and reduced immune-related pathology. These findings demonstrate that both α-crystallins contribute to persistent infection with M. tuberculosis and suggest that manipulation of acr expression can influence the host response to infection. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| Newton, Sandra M. verfasserin aut Wilkinson, Katalin A. verfasserin aut Humphreys, Ian R. oth Murphy, Helen N. oth Robertson, Brian D. oth Wilkinson, Robert J. oth Young, Douglas B. oth In Molecular microbiology Oxford [u.a.] : Wiley-Blackwell, 1987 55(2005), 4, Seite 0 Online-Ressource (DE-627)NLEJ243926537 (DE-600)1501537-3 1365-2958 nnns volume:55 year:2005 number:4 pages:0 http://dx.doi.org/10.1111/j.1365-2958.2004.04450.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 55 2005 4 0 |
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the stress-responsive chaperone α-crystallin 2 is required for pathogenesis of mycobacterium tuberculosis |
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The stress-responsive chaperone α-crystallin 2 is required for pathogenesis of Mycobacterium tuberculosis |
| abstract |
Mycobacterium tuberculosis has two members of the α-crystallin (Acr) family of molecular chaperones. Expression of Acr1 is induced by exposure to hypoxia or nitric oxide and is associated with bacterial persistence in a non-replicating state. Expression of Acr2 is induced by heat shock, oxidative stress, and uptake by macrophages. We have shown that Acr2 continues to be expressed at a high level during both acute and chronic infection in the mouse model, with an increased ratio of acr2:acr1 mRNA in the persistent phase. Deletion of the acr2 gene resulted in a decrease in the resistance of M. tuberculosis to oxidative stress but did not impair growth in mouse bone marrow macrophages. There was no difference in bacterial load in mice infected with an acr2 deletion mutant, but a marked alteration in disease progression was evident from reduced weight loss over a prolonged infection. This correlated with reduced recruitment of T-cells and macrophages to the lungs of mice infected with the acr2 mutant and reduced immune-related pathology. These findings demonstrate that both α-crystallins contribute to persistent infection with M. tuberculosis and suggest that manipulation of acr expression can influence the host response to infection. |
| abstractGer |
Mycobacterium tuberculosis has two members of the α-crystallin (Acr) family of molecular chaperones. Expression of Acr1 is induced by exposure to hypoxia or nitric oxide and is associated with bacterial persistence in a non-replicating state. Expression of Acr2 is induced by heat shock, oxidative stress, and uptake by macrophages. We have shown that Acr2 continues to be expressed at a high level during both acute and chronic infection in the mouse model, with an increased ratio of acr2:acr1 mRNA in the persistent phase. Deletion of the acr2 gene resulted in a decrease in the resistance of M. tuberculosis to oxidative stress but did not impair growth in mouse bone marrow macrophages. There was no difference in bacterial load in mice infected with an acr2 deletion mutant, but a marked alteration in disease progression was evident from reduced weight loss over a prolonged infection. This correlated with reduced recruitment of T-cells and macrophages to the lungs of mice infected with the acr2 mutant and reduced immune-related pathology. These findings demonstrate that both α-crystallins contribute to persistent infection with M. tuberculosis and suggest that manipulation of acr expression can influence the host response to infection. |
| abstract_unstemmed |
Mycobacterium tuberculosis has two members of the α-crystallin (Acr) family of molecular chaperones. Expression of Acr1 is induced by exposure to hypoxia or nitric oxide and is associated with bacterial persistence in a non-replicating state. Expression of Acr2 is induced by heat shock, oxidative stress, and uptake by macrophages. We have shown that Acr2 continues to be expressed at a high level during both acute and chronic infection in the mouse model, with an increased ratio of acr2:acr1 mRNA in the persistent phase. Deletion of the acr2 gene resulted in a decrease in the resistance of M. tuberculosis to oxidative stress but did not impair growth in mouse bone marrow macrophages. There was no difference in bacterial load in mice infected with an acr2 deletion mutant, but a marked alteration in disease progression was evident from reduced weight loss over a prolonged infection. This correlated with reduced recruitment of T-cells and macrophages to the lungs of mice infected with the acr2 mutant and reduced immune-related pathology. These findings demonstrate that both α-crystallins contribute to persistent infection with M. tuberculosis and suggest that manipulation of acr expression can influence the host response to infection. |
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The stress-responsive chaperone α-crystallin 2 is required for pathogenesis of Mycobacterium tuberculosis |
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Newton, Sandra M. Wilkinson, Katalin A. Humphreys, Ian R. Murphy, Helen N. Robertson, Brian D. Wilkinson, Robert J. Young, Douglas B. |
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Newton, Sandra M. Wilkinson, Katalin A. Humphreys, Ian R. Murphy, Helen N. Robertson, Brian D. Wilkinson, Robert J. Young, Douglas B. |
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