Chlamydophila pneumoniae induces a sustained airway hyperresponsiveness and inflammation in mice

Background It has been reported that Chlamydophila (C.) pneumoniae is involved in the initiation and promotion of asthma and chronic obstructive pulmonary diseases (COPD). Surprisingly, the effect of C. pneumoniae on airway function has never been investigated. Methods In this study, mice were inocu...
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Autor*in:	Blasi, Francesco [verfasserIn] Aliberti, Stefano Allegra, Luigi Piatti, Gioia Tarsia, Paolo Ossewaarde, Jacobus M Verweij, Vivienne Nijkamp, Frans P Folkerts, Gert

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2007

Schlagwörter:	Chronic Obstructive Pulmonary Disease Chronic Obstructive Pulmonary Disease Patient Airway Hyperresponsiveness Airway Responsiveness Telithromycin

Anmerkung:	© Blasi et al. 2007

Übergeordnetes Werk:	Enthalten in: Respiratory research - London : BioMed Central, 2001, 8(2007), 1 vom: 19. Nov.
Übergeordnetes Werk:	volume:8 ; year:2007 ; number:1 ; day:19 ; month:11

Links:	Volltext

DOI / URN:	10.1186/1465-9921-8-83

Katalog-ID:	SPR028507479

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520			\|a Background It has been reported that Chlamydophila (C.) pneumoniae is involved in the initiation and promotion of asthma and chronic obstructive pulmonary diseases (COPD). Surprisingly, the effect of C. pneumoniae on airway function has never been investigated. Methods In this study, mice were inoculated intranasally with C. pneumoniae (strain AR39) on day 0 and experiments were performed on day 2, 7, 14 and 21. Results We found that from day 7, C. pneumoniae infection causes both a sustained airway hyperresponsiveness and an inflammation. Interferon-γ (IFN-γ) and macrophage inflammatory chemokine-2 (MIP-2) levels in bronchoalveolar lavage (BAL)-fluid were increased on all experimental days with exception of day 7 where MIP-2 concentrations dropped to control levels. In contrast, tumor necrosis factor-α (TNF-α) levels were only increased on day 7. From day 7 to 21 epithelial damage and secretory cell hypertrophy was observed. It is suggested that, the inflammatory cells/mediators, the epithelial damage and secretory cell hypertrophy contribute to initiation of airway hyperresponsiveness. Conclusion Our study demonstrates for the first time that C. pneumoniae infection can modify bronchial responsiveness. This has clinical implications, since additional changes in airway responsiveness and inflammation-status induced by this bacterium may worsen and/or provoke breathlessness in asthma and COPD.
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allfields	10.1186/1465-9921-8-83 doi (DE-627)SPR028507479 (SPR)1465-9921-8-83-e DE-627 ger DE-627 rakwb eng Blasi, Francesco verfasserin aut Chlamydophila pneumoniae induces a sustained airway hyperresponsiveness and inflammation in mice 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Blasi et al. 2007 Background It has been reported that Chlamydophila (C.) pneumoniae is involved in the initiation and promotion of asthma and chronic obstructive pulmonary diseases (COPD). Surprisingly, the effect of C. pneumoniae on airway function has never been investigated. Methods In this study, mice were inoculated intranasally with C. pneumoniae (strain AR39) on day 0 and experiments were performed on day 2, 7, 14 and 21. Results We found that from day 7, C. pneumoniae infection causes both a sustained airway hyperresponsiveness and an inflammation. Interferon-γ (IFN-γ) and macrophage inflammatory chemokine-2 (MIP-2) levels in bronchoalveolar lavage (BAL)-fluid were increased on all experimental days with exception of day 7 where MIP-2 concentrations dropped to control levels. In contrast, tumor necrosis factor-α (TNF-α) levels were only increased on day 7. From day 7 to 21 epithelial damage and secretory cell hypertrophy was observed. It is suggested that, the inflammatory cells/mediators, the epithelial damage and secretory cell hypertrophy contribute to initiation of airway hyperresponsiveness. Conclusion Our study demonstrates for the first time that C. pneumoniae infection can modify bronchial responsiveness. This has clinical implications, since additional changes in airway responsiveness and inflammation-status induced by this bacterium may worsen and/or provoke breathlessness in asthma and COPD. Chronic Obstructive Pulmonary Disease (dpeaa)DE-He213 Chronic Obstructive Pulmonary Disease Patient (dpeaa)DE-He213 Airway Hyperresponsiveness (dpeaa)DE-He213 Airway Responsiveness (dpeaa)DE-He213 Telithromycin (dpeaa)DE-He213 Aliberti, Stefano aut Allegra, Luigi aut Piatti, Gioia aut Tarsia, Paolo aut Ossewaarde, Jacobus M aut Verweij, Vivienne aut Nijkamp, Frans P aut Folkerts, Gert aut Enthalten in Respiratory research London : BioMed Central, 2001 8(2007), 1 vom: 19. Nov. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:8 year:2007 number:1 day:19 month:11 https://dx.doi.org/10.1186/1465-9921-8-83 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 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_2153 GBV_ILN_2190 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2007 1 19 11
spelling	10.1186/1465-9921-8-83 doi (DE-627)SPR028507479 (SPR)1465-9921-8-83-e DE-627 ger DE-627 rakwb eng Blasi, Francesco verfasserin aut Chlamydophila pneumoniae induces a sustained airway hyperresponsiveness and inflammation in mice 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Blasi et al. 2007 Background It has been reported that Chlamydophila (C.) pneumoniae is involved in the initiation and promotion of asthma and chronic obstructive pulmonary diseases (COPD). Surprisingly, the effect of C. pneumoniae on airway function has never been investigated. Methods In this study, mice were inoculated intranasally with C. pneumoniae (strain AR39) on day 0 and experiments were performed on day 2, 7, 14 and 21. Results We found that from day 7, C. pneumoniae infection causes both a sustained airway hyperresponsiveness and an inflammation. Interferon-γ (IFN-γ) and macrophage inflammatory chemokine-2 (MIP-2) levels in bronchoalveolar lavage (BAL)-fluid were increased on all experimental days with exception of day 7 where MIP-2 concentrations dropped to control levels. In contrast, tumor necrosis factor-α (TNF-α) levels were only increased on day 7. From day 7 to 21 epithelial damage and secretory cell hypertrophy was observed. It is suggested that, the inflammatory cells/mediators, the epithelial damage and secretory cell hypertrophy contribute to initiation of airway hyperresponsiveness. Conclusion Our study demonstrates for the first time that C. pneumoniae infection can modify bronchial responsiveness. This has clinical implications, since additional changes in airway responsiveness and inflammation-status induced by this bacterium may worsen and/or provoke breathlessness in asthma and COPD. Chronic Obstructive Pulmonary Disease (dpeaa)DE-He213 Chronic Obstructive Pulmonary Disease Patient (dpeaa)DE-He213 Airway Hyperresponsiveness (dpeaa)DE-He213 Airway Responsiveness (dpeaa)DE-He213 Telithromycin (dpeaa)DE-He213 Aliberti, Stefano aut Allegra, Luigi aut Piatti, Gioia aut Tarsia, Paolo aut Ossewaarde, Jacobus M aut Verweij, Vivienne aut Nijkamp, Frans P aut Folkerts, Gert aut Enthalten in Respiratory research London : BioMed Central, 2001 8(2007), 1 vom: 19. Nov. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:8 year:2007 number:1 day:19 month:11 https://dx.doi.org/10.1186/1465-9921-8-83 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 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_2153 GBV_ILN_2190 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2007 1 19 11
allfields_unstemmed	10.1186/1465-9921-8-83 doi (DE-627)SPR028507479 (SPR)1465-9921-8-83-e DE-627 ger DE-627 rakwb eng Blasi, Francesco verfasserin aut Chlamydophila pneumoniae induces a sustained airway hyperresponsiveness and inflammation in mice 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Blasi et al. 2007 Background It has been reported that Chlamydophila (C.) pneumoniae is involved in the initiation and promotion of asthma and chronic obstructive pulmonary diseases (COPD). Surprisingly, the effect of C. pneumoniae on airway function has never been investigated. Methods In this study, mice were inoculated intranasally with C. pneumoniae (strain AR39) on day 0 and experiments were performed on day 2, 7, 14 and 21. Results We found that from day 7, C. pneumoniae infection causes both a sustained airway hyperresponsiveness and an inflammation. Interferon-γ (IFN-γ) and macrophage inflammatory chemokine-2 (MIP-2) levels in bronchoalveolar lavage (BAL)-fluid were increased on all experimental days with exception of day 7 where MIP-2 concentrations dropped to control levels. In contrast, tumor necrosis factor-α (TNF-α) levels were only increased on day 7. From day 7 to 21 epithelial damage and secretory cell hypertrophy was observed. It is suggested that, the inflammatory cells/mediators, the epithelial damage and secretory cell hypertrophy contribute to initiation of airway hyperresponsiveness. Conclusion Our study demonstrates for the first time that C. pneumoniae infection can modify bronchial responsiveness. This has clinical implications, since additional changes in airway responsiveness and inflammation-status induced by this bacterium may worsen and/or provoke breathlessness in asthma and COPD. Chronic Obstructive Pulmonary Disease (dpeaa)DE-He213 Chronic Obstructive Pulmonary Disease Patient (dpeaa)DE-He213 Airway Hyperresponsiveness (dpeaa)DE-He213 Airway Responsiveness (dpeaa)DE-He213 Telithromycin (dpeaa)DE-He213 Aliberti, Stefano aut Allegra, Luigi aut Piatti, Gioia aut Tarsia, Paolo aut Ossewaarde, Jacobus M aut Verweij, Vivienne aut Nijkamp, Frans P aut Folkerts, Gert aut Enthalten in Respiratory research London : BioMed Central, 2001 8(2007), 1 vom: 19. Nov. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:8 year:2007 number:1 day:19 month:11 https://dx.doi.org/10.1186/1465-9921-8-83 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 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_2153 GBV_ILN_2190 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2007 1 19 11
allfieldsGer	10.1186/1465-9921-8-83 doi (DE-627)SPR028507479 (SPR)1465-9921-8-83-e DE-627 ger DE-627 rakwb eng Blasi, Francesco verfasserin aut Chlamydophila pneumoniae induces a sustained airway hyperresponsiveness and inflammation in mice 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Blasi et al. 2007 Background It has been reported that Chlamydophila (C.) pneumoniae is involved in the initiation and promotion of asthma and chronic obstructive pulmonary diseases (COPD). Surprisingly, the effect of C. pneumoniae on airway function has never been investigated. Methods In this study, mice were inoculated intranasally with C. pneumoniae (strain AR39) on day 0 and experiments were performed on day 2, 7, 14 and 21. Results We found that from day 7, C. pneumoniae infection causes both a sustained airway hyperresponsiveness and an inflammation. Interferon-γ (IFN-γ) and macrophage inflammatory chemokine-2 (MIP-2) levels in bronchoalveolar lavage (BAL)-fluid were increased on all experimental days with exception of day 7 where MIP-2 concentrations dropped to control levels. In contrast, tumor necrosis factor-α (TNF-α) levels were only increased on day 7. From day 7 to 21 epithelial damage and secretory cell hypertrophy was observed. It is suggested that, the inflammatory cells/mediators, the epithelial damage and secretory cell hypertrophy contribute to initiation of airway hyperresponsiveness. Conclusion Our study demonstrates for the first time that C. pneumoniae infection can modify bronchial responsiveness. This has clinical implications, since additional changes in airway responsiveness and inflammation-status induced by this bacterium may worsen and/or provoke breathlessness in asthma and COPD. Chronic Obstructive Pulmonary Disease (dpeaa)DE-He213 Chronic Obstructive Pulmonary Disease Patient (dpeaa)DE-He213 Airway Hyperresponsiveness (dpeaa)DE-He213 Airway Responsiveness (dpeaa)DE-He213 Telithromycin (dpeaa)DE-He213 Aliberti, Stefano aut Allegra, Luigi aut Piatti, Gioia aut Tarsia, Paolo aut Ossewaarde, Jacobus M aut Verweij, Vivienne aut Nijkamp, Frans P aut Folkerts, Gert aut Enthalten in Respiratory research London : BioMed Central, 2001 8(2007), 1 vom: 19. Nov. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:8 year:2007 number:1 day:19 month:11 https://dx.doi.org/10.1186/1465-9921-8-83 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 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_2153 GBV_ILN_2190 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2007 1 19 11
allfieldsSound	10.1186/1465-9921-8-83 doi (DE-627)SPR028507479 (SPR)1465-9921-8-83-e DE-627 ger DE-627 rakwb eng Blasi, Francesco verfasserin aut Chlamydophila pneumoniae induces a sustained airway hyperresponsiveness and inflammation in mice 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Blasi et al. 2007 Background It has been reported that Chlamydophila (C.) pneumoniae is involved in the initiation and promotion of asthma and chronic obstructive pulmonary diseases (COPD). Surprisingly, the effect of C. pneumoniae on airway function has never been investigated. Methods In this study, mice were inoculated intranasally with C. pneumoniae (strain AR39) on day 0 and experiments were performed on day 2, 7, 14 and 21. Results We found that from day 7, C. pneumoniae infection causes both a sustained airway hyperresponsiveness and an inflammation. Interferon-γ (IFN-γ) and macrophage inflammatory chemokine-2 (MIP-2) levels in bronchoalveolar lavage (BAL)-fluid were increased on all experimental days with exception of day 7 where MIP-2 concentrations dropped to control levels. In contrast, tumor necrosis factor-α (TNF-α) levels were only increased on day 7. From day 7 to 21 epithelial damage and secretory cell hypertrophy was observed. It is suggested that, the inflammatory cells/mediators, the epithelial damage and secretory cell hypertrophy contribute to initiation of airway hyperresponsiveness. Conclusion Our study demonstrates for the first time that C. pneumoniae infection can modify bronchial responsiveness. This has clinical implications, since additional changes in airway responsiveness and inflammation-status induced by this bacterium may worsen and/or provoke breathlessness in asthma and COPD. Chronic Obstructive Pulmonary Disease (dpeaa)DE-He213 Chronic Obstructive Pulmonary Disease Patient (dpeaa)DE-He213 Airway Hyperresponsiveness (dpeaa)DE-He213 Airway Responsiveness (dpeaa)DE-He213 Telithromycin (dpeaa)DE-He213 Aliberti, Stefano aut Allegra, Luigi aut Piatti, Gioia aut Tarsia, Paolo aut Ossewaarde, Jacobus M aut Verweij, Vivienne aut Nijkamp, Frans P aut Folkerts, Gert aut Enthalten in Respiratory research London : BioMed Central, 2001 8(2007), 1 vom: 19. Nov. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:8 year:2007 number:1 day:19 month:11 https://dx.doi.org/10.1186/1465-9921-8-83 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 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_2153 GBV_ILN_2190 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2007 1 19 11
language	English
source	Enthalten in Respiratory research 8(2007), 1 vom: 19. Nov. volume:8 year:2007 number:1 day:19 month:11
sourceStr	Enthalten in Respiratory research 8(2007), 1 vom: 19. Nov. volume:8 year:2007 number:1 day:19 month:11
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Chronic Obstructive Pulmonary Disease Chronic Obstructive Pulmonary Disease Patient Airway Hyperresponsiveness Airway Responsiveness Telithromycin
isfreeaccess_bool	true
container_title	Respiratory research
authorswithroles_txt_mv	Blasi, Francesco @@aut@@ Aliberti, Stefano @@aut@@ Allegra, Luigi @@aut@@ Piatti, Gioia @@aut@@ Tarsia, Paolo @@aut@@ Ossewaarde, Jacobus M @@aut@@ Verweij, Vivienne @@aut@@ Nijkamp, Frans P @@aut@@ Folkerts, Gert @@aut@@
publishDateDaySort_date	2007-11-19T00:00:00Z
hierarchy_top_id	326646485
id	SPR028507479
language_de	englisch
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author	Blasi, Francesco
spellingShingle	Blasi, Francesco misc Chronic Obstructive Pulmonary Disease misc Chronic Obstructive Pulmonary Disease Patient misc Airway Hyperresponsiveness misc Airway Responsiveness misc Telithromycin Chlamydophila pneumoniae induces a sustained airway hyperresponsiveness and inflammation in mice
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topic_title	Chlamydophila pneumoniae induces a sustained airway hyperresponsiveness and inflammation in mice Chronic Obstructive Pulmonary Disease (dpeaa)DE-He213 Chronic Obstructive Pulmonary Disease Patient (dpeaa)DE-He213 Airway Hyperresponsiveness (dpeaa)DE-He213 Airway Responsiveness (dpeaa)DE-He213 Telithromycin (dpeaa)DE-He213
topic	misc Chronic Obstructive Pulmonary Disease misc Chronic Obstructive Pulmonary Disease Patient misc Airway Hyperresponsiveness misc Airway Responsiveness misc Telithromycin
topic_unstemmed	misc Chronic Obstructive Pulmonary Disease misc Chronic Obstructive Pulmonary Disease Patient misc Airway Hyperresponsiveness misc Airway Responsiveness misc Telithromycin
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title	Chlamydophila pneumoniae induces a sustained airway hyperresponsiveness and inflammation in mice
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title_full	Chlamydophila pneumoniae induces a sustained airway hyperresponsiveness and inflammation in mice
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author_browse	Blasi, Francesco Aliberti, Stefano Allegra, Luigi Piatti, Gioia Tarsia, Paolo Ossewaarde, Jacobus M Verweij, Vivienne Nijkamp, Frans P Folkerts, Gert
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title_sort	chlamydophila pneumoniae induces a sustained airway hyperresponsiveness and inflammation in mice
title_auth	Chlamydophila pneumoniae induces a sustained airway hyperresponsiveness and inflammation in mice
abstract	Background It has been reported that Chlamydophila (C.) pneumoniae is involved in the initiation and promotion of asthma and chronic obstructive pulmonary diseases (COPD). Surprisingly, the effect of C. pneumoniae on airway function has never been investigated. Methods In this study, mice were inoculated intranasally with C. pneumoniae (strain AR39) on day 0 and experiments were performed on day 2, 7, 14 and 21. Results We found that from day 7, C. pneumoniae infection causes both a sustained airway hyperresponsiveness and an inflammation. Interferon-γ (IFN-γ) and macrophage inflammatory chemokine-2 (MIP-2) levels in bronchoalveolar lavage (BAL)-fluid were increased on all experimental days with exception of day 7 where MIP-2 concentrations dropped to control levels. In contrast, tumor necrosis factor-α (TNF-α) levels were only increased on day 7. From day 7 to 21 epithelial damage and secretory cell hypertrophy was observed. It is suggested that, the inflammatory cells/mediators, the epithelial damage and secretory cell hypertrophy contribute to initiation of airway hyperresponsiveness. Conclusion Our study demonstrates for the first time that C. pneumoniae infection can modify bronchial responsiveness. This has clinical implications, since additional changes in airway responsiveness and inflammation-status induced by this bacterium may worsen and/or provoke breathlessness in asthma and COPD. © Blasi et al. 2007
abstractGer	Background It has been reported that Chlamydophila (C.) pneumoniae is involved in the initiation and promotion of asthma and chronic obstructive pulmonary diseases (COPD). Surprisingly, the effect of C. pneumoniae on airway function has never been investigated. Methods In this study, mice were inoculated intranasally with C. pneumoniae (strain AR39) on day 0 and experiments were performed on day 2, 7, 14 and 21. Results We found that from day 7, C. pneumoniae infection causes both a sustained airway hyperresponsiveness and an inflammation. Interferon-γ (IFN-γ) and macrophage inflammatory chemokine-2 (MIP-2) levels in bronchoalveolar lavage (BAL)-fluid were increased on all experimental days with exception of day 7 where MIP-2 concentrations dropped to control levels. In contrast, tumor necrosis factor-α (TNF-α) levels were only increased on day 7. From day 7 to 21 epithelial damage and secretory cell hypertrophy was observed. It is suggested that, the inflammatory cells/mediators, the epithelial damage and secretory cell hypertrophy contribute to initiation of airway hyperresponsiveness. Conclusion Our study demonstrates for the first time that C. pneumoniae infection can modify bronchial responsiveness. This has clinical implications, since additional changes in airway responsiveness and inflammation-status induced by this bacterium may worsen and/or provoke breathlessness in asthma and COPD. © Blasi et al. 2007
abstract_unstemmed	Background It has been reported that Chlamydophila (C.) pneumoniae is involved in the initiation and promotion of asthma and chronic obstructive pulmonary diseases (COPD). Surprisingly, the effect of C. pneumoniae on airway function has never been investigated. Methods In this study, mice were inoculated intranasally with C. pneumoniae (strain AR39) on day 0 and experiments were performed on day 2, 7, 14 and 21. Results We found that from day 7, C. pneumoniae infection causes both a sustained airway hyperresponsiveness and an inflammation. Interferon-γ (IFN-γ) and macrophage inflammatory chemokine-2 (MIP-2) levels in bronchoalveolar lavage (BAL)-fluid were increased on all experimental days with exception of day 7 where MIP-2 concentrations dropped to control levels. In contrast, tumor necrosis factor-α (TNF-α) levels were only increased on day 7. From day 7 to 21 epithelial damage and secretory cell hypertrophy was observed. It is suggested that, the inflammatory cells/mediators, the epithelial damage and secretory cell hypertrophy contribute to initiation of airway hyperresponsiveness. Conclusion Our study demonstrates for the first time that C. pneumoniae infection can modify bronchial responsiveness. This has clinical implications, since additional changes in airway responsiveness and inflammation-status induced by this bacterium may worsen and/or provoke breathlessness in asthma and COPD. © Blasi et al. 2007
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title_short	Chlamydophila pneumoniae induces a sustained airway hyperresponsiveness and inflammation in mice
url	https://dx.doi.org/10.1186/1465-9921-8-83
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author2	Aliberti, Stefano Allegra, Luigi Piatti, Gioia Tarsia, Paolo Ossewaarde, Jacobus M Verweij, Vivienne Nijkamp, Frans P Folkerts, Gert
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Chlamydophila pneumoniae induces a sustained airway hyperresponsiveness and inflammation in mice

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