cIAP-1 controls innate immunity to C. pneumoniae pulmonary infection.

The resistance of epithelial cells infected with Chlamydophila pneumoniae for apoptosis has been attributed to the induced expression and increased stability of anti-apoptotic proteins called inhibitor of apoptosis proteins (IAPs). The significance of cellular inhibitor of apoptosis protein-1 (cIAP-...
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Gespeichert in:

Autor*in:	Hridayesh Prakash [verfasserIn] Daniel Becker [verfasserIn] Linda Böhme [verfasserIn] Lori Albert [verfasserIn] Martin Witzenrath [verfasserIn] Simone Rosseau [verfasserIn] Thomas F Meyer [verfasserIn] Thomas Rudel [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2009

Übergeordnetes Werk:	In: PLoS ONE - Public Library of Science (PLoS), 2007, 4(2009), 8, p e6519
Übergeordnetes Werk:	volume:4 ; year:2009 ; number:8, p e6519

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1371/journal.pone.0006519

Katalog-ID:	DOAJ046465936

Internformat


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520			\|a The resistance of epithelial cells infected with Chlamydophila pneumoniae for apoptosis has been attributed to the induced expression and increased stability of anti-apoptotic proteins called inhibitor of apoptosis proteins (IAPs). The significance of cellular inhibitor of apoptosis protein-1 (cIAP-1) in C. pneumoniae pulmonary infection and innate immune response was investigated in cIAP-1 knockout (KO) mice using a novel non-invasive intra-tracheal infection method. In contrast to wildtype, cIAP-1 knockout mice failed to clear the infection from their lungs. Wildtype mice responded to infection with a strong inflammatory response in the lung. In contrast, the recruitment of macrophages was reduced in cIAP-1 KO mice compared to wildtype mice. The concentration of Interferon gamma (IFN-gamma) was increased whereas that of Tumor Necrosis Factor (TNF-alpha) was reduced in the lungs of infected cIAP-1 KO mice compared to infected wildtype mice. Ex vivo experiments on mouse peritoneal macrophages and splenocytes revealed that cIAP-1 is required for innate immune responses of these cells. Our findings thus suggest a new immunoregulatory role of cIAP-1 in the course of bacterial infection.
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912			\|a GBV_ILN_4335
912			\|a GBV_ILN_4338
912			\|a GBV_ILN_4367
912			\|a GBV_ILN_4700
951			\|a AR
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Indexfelder

author_variant	h p hp d b db l b lb l a la m w mw s r sr t f m tfm t r tr
matchkey_str	article:19326203:2009----::ipcnrlintimnttcnuoieu
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publishDate	2009
allfields	10.1371/journal.pone.0006519 doi (DE-627)DOAJ046465936 (DE-599)DOAJ1461392ff7f34aee8998bcb27169a85d DE-627 ger DE-627 rakwb eng Hridayesh Prakash verfasserin aut cIAP-1 controls innate immunity to C. pneumoniae pulmonary infection. 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The resistance of epithelial cells infected with Chlamydophila pneumoniae for apoptosis has been attributed to the induced expression and increased stability of anti-apoptotic proteins called inhibitor of apoptosis proteins (IAPs). The significance of cellular inhibitor of apoptosis protein-1 (cIAP-1) in C. pneumoniae pulmonary infection and innate immune response was investigated in cIAP-1 knockout (KO) mice using a novel non-invasive intra-tracheal infection method. In contrast to wildtype, cIAP-1 knockout mice failed to clear the infection from their lungs. Wildtype mice responded to infection with a strong inflammatory response in the lung. In contrast, the recruitment of macrophages was reduced in cIAP-1 KO mice compared to wildtype mice. The concentration of Interferon gamma (IFN-gamma) was increased whereas that of Tumor Necrosis Factor (TNF-alpha) was reduced in the lungs of infected cIAP-1 KO mice compared to infected wildtype mice. Ex vivo experiments on mouse peritoneal macrophages and splenocytes revealed that cIAP-1 is required for innate immune responses of these cells. Our findings thus suggest a new immunoregulatory role of cIAP-1 in the course of bacterial infection. Medicine R Science Q Daniel Becker verfasserin aut Linda Böhme verfasserin aut Lori Albert verfasserin aut Martin Witzenrath verfasserin aut Simone Rosseau verfasserin aut Thomas F Meyer verfasserin aut Thomas Rudel verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 4(2009), 8, p e6519 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:4 year:2009 number:8, p e6519 https://doi.org/10.1371/journal.pone.0006519 kostenfrei https://doaj.org/article/1461392ff7f34aee8998bcb27169a85d kostenfrei http://europepmc.org/articles/PMC2716518?pdf=render kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2009 8, p e6519
spelling	10.1371/journal.pone.0006519 doi (DE-627)DOAJ046465936 (DE-599)DOAJ1461392ff7f34aee8998bcb27169a85d DE-627 ger DE-627 rakwb eng Hridayesh Prakash verfasserin aut cIAP-1 controls innate immunity to C. pneumoniae pulmonary infection. 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The resistance of epithelial cells infected with Chlamydophila pneumoniae for apoptosis has been attributed to the induced expression and increased stability of anti-apoptotic proteins called inhibitor of apoptosis proteins (IAPs). The significance of cellular inhibitor of apoptosis protein-1 (cIAP-1) in C. pneumoniae pulmonary infection and innate immune response was investigated in cIAP-1 knockout (KO) mice using a novel non-invasive intra-tracheal infection method. In contrast to wildtype, cIAP-1 knockout mice failed to clear the infection from their lungs. Wildtype mice responded to infection with a strong inflammatory response in the lung. In contrast, the recruitment of macrophages was reduced in cIAP-1 KO mice compared to wildtype mice. The concentration of Interferon gamma (IFN-gamma) was increased whereas that of Tumor Necrosis Factor (TNF-alpha) was reduced in the lungs of infected cIAP-1 KO mice compared to infected wildtype mice. Ex vivo experiments on mouse peritoneal macrophages and splenocytes revealed that cIAP-1 is required for innate immune responses of these cells. Our findings thus suggest a new immunoregulatory role of cIAP-1 in the course of bacterial infection. Medicine R Science Q Daniel Becker verfasserin aut Linda Böhme verfasserin aut Lori Albert verfasserin aut Martin Witzenrath verfasserin aut Simone Rosseau verfasserin aut Thomas F Meyer verfasserin aut Thomas Rudel verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 4(2009), 8, p e6519 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:4 year:2009 number:8, p e6519 https://doi.org/10.1371/journal.pone.0006519 kostenfrei https://doaj.org/article/1461392ff7f34aee8998bcb27169a85d kostenfrei http://europepmc.org/articles/PMC2716518?pdf=render kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2009 8, p e6519
allfields_unstemmed	10.1371/journal.pone.0006519 doi (DE-627)DOAJ046465936 (DE-599)DOAJ1461392ff7f34aee8998bcb27169a85d DE-627 ger DE-627 rakwb eng Hridayesh Prakash verfasserin aut cIAP-1 controls innate immunity to C. pneumoniae pulmonary infection. 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The resistance of epithelial cells infected with Chlamydophila pneumoniae for apoptosis has been attributed to the induced expression and increased stability of anti-apoptotic proteins called inhibitor of apoptosis proteins (IAPs). The significance of cellular inhibitor of apoptosis protein-1 (cIAP-1) in C. pneumoniae pulmonary infection and innate immune response was investigated in cIAP-1 knockout (KO) mice using a novel non-invasive intra-tracheal infection method. In contrast to wildtype, cIAP-1 knockout mice failed to clear the infection from their lungs. Wildtype mice responded to infection with a strong inflammatory response in the lung. In contrast, the recruitment of macrophages was reduced in cIAP-1 KO mice compared to wildtype mice. The concentration of Interferon gamma (IFN-gamma) was increased whereas that of Tumor Necrosis Factor (TNF-alpha) was reduced in the lungs of infected cIAP-1 KO mice compared to infected wildtype mice. Ex vivo experiments on mouse peritoneal macrophages and splenocytes revealed that cIAP-1 is required for innate immune responses of these cells. Our findings thus suggest a new immunoregulatory role of cIAP-1 in the course of bacterial infection. Medicine R Science Q Daniel Becker verfasserin aut Linda Böhme verfasserin aut Lori Albert verfasserin aut Martin Witzenrath verfasserin aut Simone Rosseau verfasserin aut Thomas F Meyer verfasserin aut Thomas Rudel verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 4(2009), 8, p e6519 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:4 year:2009 number:8, p e6519 https://doi.org/10.1371/journal.pone.0006519 kostenfrei https://doaj.org/article/1461392ff7f34aee8998bcb27169a85d kostenfrei http://europepmc.org/articles/PMC2716518?pdf=render kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2009 8, p e6519
allfieldsGer	10.1371/journal.pone.0006519 doi (DE-627)DOAJ046465936 (DE-599)DOAJ1461392ff7f34aee8998bcb27169a85d DE-627 ger DE-627 rakwb eng Hridayesh Prakash verfasserin aut cIAP-1 controls innate immunity to C. pneumoniae pulmonary infection. 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The resistance of epithelial cells infected with Chlamydophila pneumoniae for apoptosis has been attributed to the induced expression and increased stability of anti-apoptotic proteins called inhibitor of apoptosis proteins (IAPs). The significance of cellular inhibitor of apoptosis protein-1 (cIAP-1) in C. pneumoniae pulmonary infection and innate immune response was investigated in cIAP-1 knockout (KO) mice using a novel non-invasive intra-tracheal infection method. In contrast to wildtype, cIAP-1 knockout mice failed to clear the infection from their lungs. Wildtype mice responded to infection with a strong inflammatory response in the lung. In contrast, the recruitment of macrophages was reduced in cIAP-1 KO mice compared to wildtype mice. The concentration of Interferon gamma (IFN-gamma) was increased whereas that of Tumor Necrosis Factor (TNF-alpha) was reduced in the lungs of infected cIAP-1 KO mice compared to infected wildtype mice. Ex vivo experiments on mouse peritoneal macrophages and splenocytes revealed that cIAP-1 is required for innate immune responses of these cells. Our findings thus suggest a new immunoregulatory role of cIAP-1 in the course of bacterial infection. Medicine R Science Q Daniel Becker verfasserin aut Linda Böhme verfasserin aut Lori Albert verfasserin aut Martin Witzenrath verfasserin aut Simone Rosseau verfasserin aut Thomas F Meyer verfasserin aut Thomas Rudel verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 4(2009), 8, p e6519 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:4 year:2009 number:8, p e6519 https://doi.org/10.1371/journal.pone.0006519 kostenfrei https://doaj.org/article/1461392ff7f34aee8998bcb27169a85d kostenfrei http://europepmc.org/articles/PMC2716518?pdf=render kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2009 8, p e6519
allfieldsSound	10.1371/journal.pone.0006519 doi (DE-627)DOAJ046465936 (DE-599)DOAJ1461392ff7f34aee8998bcb27169a85d DE-627 ger DE-627 rakwb eng Hridayesh Prakash verfasserin aut cIAP-1 controls innate immunity to C. pneumoniae pulmonary infection. 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The resistance of epithelial cells infected with Chlamydophila pneumoniae for apoptosis has been attributed to the induced expression and increased stability of anti-apoptotic proteins called inhibitor of apoptosis proteins (IAPs). The significance of cellular inhibitor of apoptosis protein-1 (cIAP-1) in C. pneumoniae pulmonary infection and innate immune response was investigated in cIAP-1 knockout (KO) mice using a novel non-invasive intra-tracheal infection method. In contrast to wildtype, cIAP-1 knockout mice failed to clear the infection from their lungs. Wildtype mice responded to infection with a strong inflammatory response in the lung. In contrast, the recruitment of macrophages was reduced in cIAP-1 KO mice compared to wildtype mice. The concentration of Interferon gamma (IFN-gamma) was increased whereas that of Tumor Necrosis Factor (TNF-alpha) was reduced in the lungs of infected cIAP-1 KO mice compared to infected wildtype mice. Ex vivo experiments on mouse peritoneal macrophages and splenocytes revealed that cIAP-1 is required for innate immune responses of these cells. Our findings thus suggest a new immunoregulatory role of cIAP-1 in the course of bacterial infection. Medicine R Science Q Daniel Becker verfasserin aut Linda Böhme verfasserin aut Lori Albert verfasserin aut Martin Witzenrath verfasserin aut Simone Rosseau verfasserin aut Thomas F Meyer verfasserin aut Thomas Rudel verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 4(2009), 8, p e6519 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:4 year:2009 number:8, p e6519 https://doi.org/10.1371/journal.pone.0006519 kostenfrei https://doaj.org/article/1461392ff7f34aee8998bcb27169a85d kostenfrei http://europepmc.org/articles/PMC2716518?pdf=render kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2009 8, p e6519
language	English
source	In PLoS ONE 4(2009), 8, p e6519 volume:4 year:2009 number:8, p e6519
sourceStr	In PLoS ONE 4(2009), 8, p e6519 volume:4 year:2009 number:8, p e6519
format_phy_str_mv	Article
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authorswithroles_txt_mv	Hridayesh Prakash @@aut@@ Daniel Becker @@aut@@ Linda Böhme @@aut@@ Lori Albert @@aut@@ Martin Witzenrath @@aut@@ Simone Rosseau @@aut@@ Thomas F Meyer @@aut@@ Thomas Rudel @@aut@@
publishDateDaySort_date	2009-01-01T00:00:00Z
hierarchy_top_id	523574592
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author	Hridayesh Prakash
spellingShingle	Hridayesh Prakash misc Medicine misc R misc Science misc Q cIAP-1 controls innate immunity to C. pneumoniae pulmonary infection.
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topic_title	cIAP-1 controls innate immunity to C. pneumoniae pulmonary infection
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title	cIAP-1 controls innate immunity to C. pneumoniae pulmonary infection.
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title_full	cIAP-1 controls innate immunity to C. pneumoniae pulmonary infection
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author_browse	Hridayesh Prakash Daniel Becker Linda Böhme Lori Albert Martin Witzenrath Simone Rosseau Thomas F Meyer Thomas Rudel
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title_sort	ciap-1 controls innate immunity to c. pneumoniae pulmonary infection
title_auth	cIAP-1 controls innate immunity to C. pneumoniae pulmonary infection.
abstract	The resistance of epithelial cells infected with Chlamydophila pneumoniae for apoptosis has been attributed to the induced expression and increased stability of anti-apoptotic proteins called inhibitor of apoptosis proteins (IAPs). The significance of cellular inhibitor of apoptosis protein-1 (cIAP-1) in C. pneumoniae pulmonary infection and innate immune response was investigated in cIAP-1 knockout (KO) mice using a novel non-invasive intra-tracheal infection method. In contrast to wildtype, cIAP-1 knockout mice failed to clear the infection from their lungs. Wildtype mice responded to infection with a strong inflammatory response in the lung. In contrast, the recruitment of macrophages was reduced in cIAP-1 KO mice compared to wildtype mice. The concentration of Interferon gamma (IFN-gamma) was increased whereas that of Tumor Necrosis Factor (TNF-alpha) was reduced in the lungs of infected cIAP-1 KO mice compared to infected wildtype mice. Ex vivo experiments on mouse peritoneal macrophages and splenocytes revealed that cIAP-1 is required for innate immune responses of these cells. Our findings thus suggest a new immunoregulatory role of cIAP-1 in the course of bacterial infection.
abstractGer	The resistance of epithelial cells infected with Chlamydophila pneumoniae for apoptosis has been attributed to the induced expression and increased stability of anti-apoptotic proteins called inhibitor of apoptosis proteins (IAPs). The significance of cellular inhibitor of apoptosis protein-1 (cIAP-1) in C. pneumoniae pulmonary infection and innate immune response was investigated in cIAP-1 knockout (KO) mice using a novel non-invasive intra-tracheal infection method. In contrast to wildtype, cIAP-1 knockout mice failed to clear the infection from their lungs. Wildtype mice responded to infection with a strong inflammatory response in the lung. In contrast, the recruitment of macrophages was reduced in cIAP-1 KO mice compared to wildtype mice. The concentration of Interferon gamma (IFN-gamma) was increased whereas that of Tumor Necrosis Factor (TNF-alpha) was reduced in the lungs of infected cIAP-1 KO mice compared to infected wildtype mice. Ex vivo experiments on mouse peritoneal macrophages and splenocytes revealed that cIAP-1 is required for innate immune responses of these cells. Our findings thus suggest a new immunoregulatory role of cIAP-1 in the course of bacterial infection.
abstract_unstemmed	The resistance of epithelial cells infected with Chlamydophila pneumoniae for apoptosis has been attributed to the induced expression and increased stability of anti-apoptotic proteins called inhibitor of apoptosis proteins (IAPs). The significance of cellular inhibitor of apoptosis protein-1 (cIAP-1) in C. pneumoniae pulmonary infection and innate immune response was investigated in cIAP-1 knockout (KO) mice using a novel non-invasive intra-tracheal infection method. In contrast to wildtype, cIAP-1 knockout mice failed to clear the infection from their lungs. Wildtype mice responded to infection with a strong inflammatory response in the lung. In contrast, the recruitment of macrophages was reduced in cIAP-1 KO mice compared to wildtype mice. The concentration of Interferon gamma (IFN-gamma) was increased whereas that of Tumor Necrosis Factor (TNF-alpha) was reduced in the lungs of infected cIAP-1 KO mice compared to infected wildtype mice. Ex vivo experiments on mouse peritoneal macrophages and splenocytes revealed that cIAP-1 is required for innate immune responses of these cells. Our findings thus suggest a new immunoregulatory role of cIAP-1 in the course of bacterial infection.
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title_short	cIAP-1 controls innate immunity to C. pneumoniae pulmonary infection.
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cIAP-1 controls innate immunity to C. pneumoniae pulmonary infection.

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