Adhesion to and biofilm formation on IB3-1 bronchial cells by <it<Stenotrophomonas maltophilia </it<isolates from cystic fibrosis patients

<p<Abstract</p< <p<Background</p< <p<<it<Stenotrophomonas maltophilia </it<has recently gained considerable attention as an important emerging pathogen in cystic fibrosis (CF) patients. However, the role of this microorganism in the pathophysiology of CF lung disease remains largely unexplored. In the present study for the first time we assessed the ability of <it<S. maltophilia </it<CF isolates to adhere to and form biofilm in experimental infection experiments using the CF-derived bronchial epithelial IB3-1cell line. The role of flagella on the adhesiveness of <it<S. maltophilia </it<to IB3-1 cell monolayers was also assessed by using <it<fliI </it<mutant derivative strains.</p< <p<Results</p< <p<All <it<S. maltophilia </it<CF isolates tested in the present study were able, although at different levels, to adhere to and form biofilm on IB3-1 cell monolayers. Scanning electron and confocal microscopy revealed <it<S. maltophilia </it<structures typical of biofilm formation on bronchial IB3-1 cells. The loss of flagella significantly (P < 0.001) decreased bacterial adhesiveness, if compared to that of their parental flagellated strains. <it<S. maltophilia </it<CF isolates were also able to invade IB3-1 cells, albeit at a very low level (internalization rate ranged from 0.01 to 4.94%). Pre-exposure of IB3-1 cells to <it<P. aeruginosa </it<PAO1 significantly increased <it<S. maltophilia </it<adhesiveness. Further, the presence of <it<S. maltophilia </it<negatively influenced <it<P. aeruginosa </it<PAO1 adhesiveness.</p< <p<Conclusions</p< <p<The main contribution of the present study is the finding that <it<S. maltophilia </it<is able to form biofilm on and invade CF-derived IB3-1 bronchial epithelial cells, thus posing a rationale for the persistence and the systemic spread of this opportunistic pathogen in CF patients. Experiments using <it<in vivo </it<models which more closely mimic CF pulmonary tissues will certainly be needed to validate the relevance of our results.</p< Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Petrucca Andrea [verfasserIn] Nicoletti Mauro [verfasserIn] Confalone Pamela [verfasserIn] Crocetta Valentina [verfasserIn] Pompilio Arianna [verfasserIn] Guarnieri Simone [verfasserIn] Fiscarelli Ersilia [verfasserIn] Savini Vincenzo [verfasserIn] Piccolomini Raffaele [verfasserIn] Di Bonaventura Giovanni [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2010

Übergeordnetes Werk:	In: BMC Microbiology - BMC, 2003, 10(2010), 1, p 102
Übergeordnetes Werk:	volume:10 ; year:2010 ; number:1, p 102

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1471-2180-10-102

Katalog-ID:	DOAJ038438011

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publishDate	2010
allfields	10.1186/1471-2180-10-102 doi (DE-627)DOAJ038438011 (DE-599)DOAJ789e96b79ffc4ce2b6bfce3808eb9511 DE-627 ger DE-627 rakwb eng QR1-502 Petrucca Andrea verfasserin aut Adhesion to and biofilm formation on IB3-1 bronchial cells by <it<Stenotrophomonas maltophilia </it<isolates from cystic fibrosis patients 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<<it<Stenotrophomonas maltophilia </it<has recently gained considerable attention as an important emerging pathogen in cystic fibrosis (CF) patients. However, the role of this microorganism in the pathophysiology of CF lung disease remains largely unexplored. In the present study for the first time we assessed the ability of <it<S. maltophilia </it<CF isolates to adhere to and form biofilm in experimental infection experiments using the CF-derived bronchial epithelial IB3-1cell line. The role of flagella on the adhesiveness of <it<S. maltophilia </it<to IB3-1 cell monolayers was also assessed by using <it<fliI </it<mutant derivative strains.</p< <p<Results</p< <p<All <it<S. maltophilia </it<CF isolates tested in the present study were able, although at different levels, to adhere to and form biofilm on IB3-1 cell monolayers. Scanning electron and confocal microscopy revealed <it<S. maltophilia </it<structures typical of biofilm formation on bronchial IB3-1 cells. The loss of flagella significantly (P < 0.001) decreased bacterial adhesiveness, if compared to that of their parental flagellated strains. <it<S. maltophilia </it<CF isolates were also able to invade IB3-1 cells, albeit at a very low level (internalization rate ranged from 0.01 to 4.94%). Pre-exposure of IB3-1 cells to <it<P. aeruginosa </it<PAO1 significantly increased <it<S. maltophilia </it<adhesiveness. Further, the presence of <it<S. maltophilia </it<negatively influenced <it<P. aeruginosa </it<PAO1 adhesiveness.</p< <p<Conclusions</p< <p<The main contribution of the present study is the finding that <it<S. maltophilia </it<is able to form biofilm on and invade CF-derived IB3-1 bronchial epithelial cells, thus posing a rationale for the persistence and the systemic spread of this opportunistic pathogen in CF patients. Experiments using <it<in vivo </it<models which more closely mimic CF pulmonary tissues will certainly be needed to validate the relevance of our results.</p< Microbiology Nicoletti Mauro verfasserin aut Confalone Pamela verfasserin aut Crocetta Valentina verfasserin aut Pompilio Arianna verfasserin aut Guarnieri Simone verfasserin aut Fiscarelli Ersilia verfasserin aut Savini Vincenzo verfasserin aut Piccolomini Raffaele verfasserin aut Di Bonaventura Giovanni verfasserin aut In BMC Microbiology BMC, 2003 10(2010), 1, p 102 (DE-627)326644997 (DE-600)2041505-9 14712180 nnns volume:10 year:2010 number:1, p 102 https://doi.org/10.1186/1471-2180-10-102 kostenfrei https://doaj.org/article/789e96b79ffc4ce2b6bfce3808eb9511 kostenfrei http://www.biomedcentral.com/1471-2180/10/102 kostenfrei https://doaj.org/toc/1471-2180 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_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_206 GBV_ILN_213 GBV_ILN_224 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_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 10 2010 1, p 102
spelling	10.1186/1471-2180-10-102 doi (DE-627)DOAJ038438011 (DE-599)DOAJ789e96b79ffc4ce2b6bfce3808eb9511 DE-627 ger DE-627 rakwb eng QR1-502 Petrucca Andrea verfasserin aut Adhesion to and biofilm formation on IB3-1 bronchial cells by <it<Stenotrophomonas maltophilia </it<isolates from cystic fibrosis patients 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<<it<Stenotrophomonas maltophilia </it<has recently gained considerable attention as an important emerging pathogen in cystic fibrosis (CF) patients. However, the role of this microorganism in the pathophysiology of CF lung disease remains largely unexplored. In the present study for the first time we assessed the ability of <it<S. maltophilia </it<CF isolates to adhere to and form biofilm in experimental infection experiments using the CF-derived bronchial epithelial IB3-1cell line. The role of flagella on the adhesiveness of <it<S. maltophilia </it<to IB3-1 cell monolayers was also assessed by using <it<fliI </it<mutant derivative strains.</p< <p<Results</p< <p<All <it<S. maltophilia </it<CF isolates tested in the present study were able, although at different levels, to adhere to and form biofilm on IB3-1 cell monolayers. Scanning electron and confocal microscopy revealed <it<S. maltophilia </it<structures typical of biofilm formation on bronchial IB3-1 cells. The loss of flagella significantly (P < 0.001) decreased bacterial adhesiveness, if compared to that of their parental flagellated strains. <it<S. maltophilia </it<CF isolates were also able to invade IB3-1 cells, albeit at a very low level (internalization rate ranged from 0.01 to 4.94%). Pre-exposure of IB3-1 cells to <it<P. aeruginosa </it<PAO1 significantly increased <it<S. maltophilia </it<adhesiveness. Further, the presence of <it<S. maltophilia </it<negatively influenced <it<P. aeruginosa </it<PAO1 adhesiveness.</p< <p<Conclusions</p< <p<The main contribution of the present study is the finding that <it<S. maltophilia </it<is able to form biofilm on and invade CF-derived IB3-1 bronchial epithelial cells, thus posing a rationale for the persistence and the systemic spread of this opportunistic pathogen in CF patients. Experiments using <it<in vivo </it<models which more closely mimic CF pulmonary tissues will certainly be needed to validate the relevance of our results.</p< Microbiology Nicoletti Mauro verfasserin aut Confalone Pamela verfasserin aut Crocetta Valentina verfasserin aut Pompilio Arianna verfasserin aut Guarnieri Simone verfasserin aut Fiscarelli Ersilia verfasserin aut Savini Vincenzo verfasserin aut Piccolomini Raffaele verfasserin aut Di Bonaventura Giovanni verfasserin aut In BMC Microbiology BMC, 2003 10(2010), 1, p 102 (DE-627)326644997 (DE-600)2041505-9 14712180 nnns volume:10 year:2010 number:1, p 102 https://doi.org/10.1186/1471-2180-10-102 kostenfrei https://doaj.org/article/789e96b79ffc4ce2b6bfce3808eb9511 kostenfrei http://www.biomedcentral.com/1471-2180/10/102 kostenfrei https://doaj.org/toc/1471-2180 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_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_206 GBV_ILN_213 GBV_ILN_224 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_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 10 2010 1, p 102
allfields_unstemmed	10.1186/1471-2180-10-102 doi (DE-627)DOAJ038438011 (DE-599)DOAJ789e96b79ffc4ce2b6bfce3808eb9511 DE-627 ger DE-627 rakwb eng QR1-502 Petrucca Andrea verfasserin aut Adhesion to and biofilm formation on IB3-1 bronchial cells by <it<Stenotrophomonas maltophilia </it<isolates from cystic fibrosis patients 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<<it<Stenotrophomonas maltophilia </it<has recently gained considerable attention as an important emerging pathogen in cystic fibrosis (CF) patients. However, the role of this microorganism in the pathophysiology of CF lung disease remains largely unexplored. In the present study for the first time we assessed the ability of <it<S. maltophilia </it<CF isolates to adhere to and form biofilm in experimental infection experiments using the CF-derived bronchial epithelial IB3-1cell line. The role of flagella on the adhesiveness of <it<S. maltophilia </it<to IB3-1 cell monolayers was also assessed by using <it<fliI </it<mutant derivative strains.</p< <p<Results</p< <p<All <it<S. maltophilia </it<CF isolates tested in the present study were able, although at different levels, to adhere to and form biofilm on IB3-1 cell monolayers. Scanning electron and confocal microscopy revealed <it<S. maltophilia </it<structures typical of biofilm formation on bronchial IB3-1 cells. The loss of flagella significantly (P < 0.001) decreased bacterial adhesiveness, if compared to that of their parental flagellated strains. <it<S. maltophilia </it<CF isolates were also able to invade IB3-1 cells, albeit at a very low level (internalization rate ranged from 0.01 to 4.94%). Pre-exposure of IB3-1 cells to <it<P. aeruginosa </it<PAO1 significantly increased <it<S. maltophilia </it<adhesiveness. Further, the presence of <it<S. maltophilia </it<negatively influenced <it<P. aeruginosa </it<PAO1 adhesiveness.</p< <p<Conclusions</p< <p<The main contribution of the present study is the finding that <it<S. maltophilia </it<is able to form biofilm on and invade CF-derived IB3-1 bronchial epithelial cells, thus posing a rationale for the persistence and the systemic spread of this opportunistic pathogen in CF patients. Experiments using <it<in vivo </it<models which more closely mimic CF pulmonary tissues will certainly be needed to validate the relevance of our results.</p< Microbiology Nicoletti Mauro verfasserin aut Confalone Pamela verfasserin aut Crocetta Valentina verfasserin aut Pompilio Arianna verfasserin aut Guarnieri Simone verfasserin aut Fiscarelli Ersilia verfasserin aut Savini Vincenzo verfasserin aut Piccolomini Raffaele verfasserin aut Di Bonaventura Giovanni verfasserin aut In BMC Microbiology BMC, 2003 10(2010), 1, p 102 (DE-627)326644997 (DE-600)2041505-9 14712180 nnns volume:10 year:2010 number:1, p 102 https://doi.org/10.1186/1471-2180-10-102 kostenfrei https://doaj.org/article/789e96b79ffc4ce2b6bfce3808eb9511 kostenfrei http://www.biomedcentral.com/1471-2180/10/102 kostenfrei https://doaj.org/toc/1471-2180 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_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_206 GBV_ILN_213 GBV_ILN_224 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_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 10 2010 1, p 102
allfieldsGer	10.1186/1471-2180-10-102 doi (DE-627)DOAJ038438011 (DE-599)DOAJ789e96b79ffc4ce2b6bfce3808eb9511 DE-627 ger DE-627 rakwb eng QR1-502 Petrucca Andrea verfasserin aut Adhesion to and biofilm formation on IB3-1 bronchial cells by <it<Stenotrophomonas maltophilia </it<isolates from cystic fibrosis patients 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<<it<Stenotrophomonas maltophilia </it<has recently gained considerable attention as an important emerging pathogen in cystic fibrosis (CF) patients. However, the role of this microorganism in the pathophysiology of CF lung disease remains largely unexplored. In the present study for the first time we assessed the ability of <it<S. maltophilia </it<CF isolates to adhere to and form biofilm in experimental infection experiments using the CF-derived bronchial epithelial IB3-1cell line. The role of flagella on the adhesiveness of <it<S. maltophilia </it<to IB3-1 cell monolayers was also assessed by using <it<fliI </it<mutant derivative strains.</p< <p<Results</p< <p<All <it<S. maltophilia </it<CF isolates tested in the present study were able, although at different levels, to adhere to and form biofilm on IB3-1 cell monolayers. Scanning electron and confocal microscopy revealed <it<S. maltophilia </it<structures typical of biofilm formation on bronchial IB3-1 cells. The loss of flagella significantly (P < 0.001) decreased bacterial adhesiveness, if compared to that of their parental flagellated strains. <it<S. maltophilia </it<CF isolates were also able to invade IB3-1 cells, albeit at a very low level (internalization rate ranged from 0.01 to 4.94%). Pre-exposure of IB3-1 cells to <it<P. aeruginosa </it<PAO1 significantly increased <it<S. maltophilia </it<adhesiveness. Further, the presence of <it<S. maltophilia </it<negatively influenced <it<P. aeruginosa </it<PAO1 adhesiveness.</p< <p<Conclusions</p< <p<The main contribution of the present study is the finding that <it<S. maltophilia </it<is able to form biofilm on and invade CF-derived IB3-1 bronchial epithelial cells, thus posing a rationale for the persistence and the systemic spread of this opportunistic pathogen in CF patients. Experiments using <it<in vivo </it<models which more closely mimic CF pulmonary tissues will certainly be needed to validate the relevance of our results.</p< Microbiology Nicoletti Mauro verfasserin aut Confalone Pamela verfasserin aut Crocetta Valentina verfasserin aut Pompilio Arianna verfasserin aut Guarnieri Simone verfasserin aut Fiscarelli Ersilia verfasserin aut Savini Vincenzo verfasserin aut Piccolomini Raffaele verfasserin aut Di Bonaventura Giovanni verfasserin aut In BMC Microbiology BMC, 2003 10(2010), 1, p 102 (DE-627)326644997 (DE-600)2041505-9 14712180 nnns volume:10 year:2010 number:1, p 102 https://doi.org/10.1186/1471-2180-10-102 kostenfrei https://doaj.org/article/789e96b79ffc4ce2b6bfce3808eb9511 kostenfrei http://www.biomedcentral.com/1471-2180/10/102 kostenfrei https://doaj.org/toc/1471-2180 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_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_206 GBV_ILN_213 GBV_ILN_224 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_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 10 2010 1, p 102
allfieldsSound	10.1186/1471-2180-10-102 doi (DE-627)DOAJ038438011 (DE-599)DOAJ789e96b79ffc4ce2b6bfce3808eb9511 DE-627 ger DE-627 rakwb eng QR1-502 Petrucca Andrea verfasserin aut Adhesion to and biofilm formation on IB3-1 bronchial cells by <it<Stenotrophomonas maltophilia </it<isolates from cystic fibrosis patients 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<<it<Stenotrophomonas maltophilia </it<has recently gained considerable attention as an important emerging pathogen in cystic fibrosis (CF) patients. However, the role of this microorganism in the pathophysiology of CF lung disease remains largely unexplored. In the present study for the first time we assessed the ability of <it<S. maltophilia </it<CF isolates to adhere to and form biofilm in experimental infection experiments using the CF-derived bronchial epithelial IB3-1cell line. The role of flagella on the adhesiveness of <it<S. maltophilia </it<to IB3-1 cell monolayers was also assessed by using <it<fliI </it<mutant derivative strains.</p< <p<Results</p< <p<All <it<S. maltophilia </it<CF isolates tested in the present study were able, although at different levels, to adhere to and form biofilm on IB3-1 cell monolayers. Scanning electron and confocal microscopy revealed <it<S. maltophilia </it<structures typical of biofilm formation on bronchial IB3-1 cells. The loss of flagella significantly (P < 0.001) decreased bacterial adhesiveness, if compared to that of their parental flagellated strains. <it<S. maltophilia </it<CF isolates were also able to invade IB3-1 cells, albeit at a very low level (internalization rate ranged from 0.01 to 4.94%). Pre-exposure of IB3-1 cells to <it<P. aeruginosa </it<PAO1 significantly increased <it<S. maltophilia </it<adhesiveness. Further, the presence of <it<S. maltophilia </it<negatively influenced <it<P. aeruginosa </it<PAO1 adhesiveness.</p< <p<Conclusions</p< <p<The main contribution of the present study is the finding that <it<S. maltophilia </it<is able to form biofilm on and invade CF-derived IB3-1 bronchial epithelial cells, thus posing a rationale for the persistence and the systemic spread of this opportunistic pathogen in CF patients. Experiments using <it<in vivo </it<models which more closely mimic CF pulmonary tissues will certainly be needed to validate the relevance of our results.</p< Microbiology Nicoletti Mauro verfasserin aut Confalone Pamela verfasserin aut Crocetta Valentina verfasserin aut Pompilio Arianna verfasserin aut Guarnieri Simone verfasserin aut Fiscarelli Ersilia verfasserin aut Savini Vincenzo verfasserin aut Piccolomini Raffaele verfasserin aut Di Bonaventura Giovanni verfasserin aut In BMC Microbiology BMC, 2003 10(2010), 1, p 102 (DE-627)326644997 (DE-600)2041505-9 14712180 nnns volume:10 year:2010 number:1, p 102 https://doi.org/10.1186/1471-2180-10-102 kostenfrei https://doaj.org/article/789e96b79ffc4ce2b6bfce3808eb9511 kostenfrei http://www.biomedcentral.com/1471-2180/10/102 kostenfrei https://doaj.org/toc/1471-2180 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_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_206 GBV_ILN_213 GBV_ILN_224 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_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 10 2010 1, p 102
language	English
source	In BMC Microbiology 10(2010), 1, p 102 volume:10 year:2010 number:1, p 102
sourceStr	In BMC Microbiology 10(2010), 1, p 102 volume:10 year:2010 number:1, p 102
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Microbiology
isfreeaccess_bool	true
container_title	BMC Microbiology
authorswithroles_txt_mv	Petrucca Andrea @@aut@@ Nicoletti Mauro @@aut@@ Confalone Pamela @@aut@@ Crocetta Valentina @@aut@@ Pompilio Arianna @@aut@@ Guarnieri Simone @@aut@@ Fiscarelli Ersilia @@aut@@ Savini Vincenzo @@aut@@ Piccolomini Raffaele @@aut@@ Di Bonaventura Giovanni @@aut@@
publishDateDaySort_date	2010-01-01T00:00:00Z
hierarchy_top_id	326644997
id	DOAJ038438011
language_de	englisch
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However, the role of this microorganism in the pathophysiology of CF lung disease remains largely unexplored. In the present study for the first time we assessed the ability of <it<S. maltophilia </it<CF isolates to adhere to and form biofilm in experimental infection experiments using the CF-derived bronchial epithelial IB3-1cell line. The role of flagella on the adhesiveness of <it<S. maltophilia </it<to IB3-1 cell monolayers was also assessed by using <it<fliI </it<mutant derivative strains.</p< <p<Results</p< <p<All <it<S. maltophilia </it<CF isolates tested in the present study were able, although at different levels, to adhere to and form biofilm on IB3-1 cell monolayers. Scanning electron and confocal microscopy revealed <it<S. maltophilia </it<structures typical of biofilm formation on bronchial IB3-1 cells. The loss of flagella significantly (P < 0.001) decreased bacterial adhesiveness, if compared to that of their parental flagellated strains. <it<S. maltophilia </it<CF isolates were also able to invade IB3-1 cells, albeit at a very low level (internalization rate ranged from 0.01 to 4.94%). Pre-exposure of IB3-1 cells to <it<P. aeruginosa </it<PAO1 significantly increased <it<S. maltophilia </it<adhesiveness. Further, the presence of <it<S. maltophilia </it<negatively influenced <it<P. aeruginosa </it<PAO1 adhesiveness.</p< <p<Conclusions</p< <p<The main contribution of the present study is the finding that <it<S. maltophilia </it<is able to form biofilm on and invade CF-derived IB3-1 bronchial epithelial cells, thus posing a rationale for the persistence and the systemic spread of this opportunistic pathogen in CF patients. 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callnumber-first	Q - Science
author	Petrucca Andrea
spellingShingle	Petrucca Andrea misc QR1-502 misc Microbiology Adhesion to and biofilm formation on IB3-1 bronchial cells by <it<Stenotrophomonas maltophilia </it<isolates from cystic fibrosis patients
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topic_title	QR1-502 Adhesion to and biofilm formation on IB3-1 bronchial cells by <it<Stenotrophomonas maltophilia </it<isolates from cystic fibrosis patients
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title	Adhesion to and biofilm formation on IB3-1 bronchial cells by <it<Stenotrophomonas maltophilia </it<isolates from cystic fibrosis patients
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title_full	Adhesion to and biofilm formation on IB3-1 bronchial cells by <it<Stenotrophomonas maltophilia </it<isolates from cystic fibrosis patients
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author_browse	Petrucca Andrea Nicoletti Mauro Confalone Pamela Crocetta Valentina Pompilio Arianna Guarnieri Simone Fiscarelli Ersilia Savini Vincenzo Piccolomini Raffaele Di Bonaventura Giovanni
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title_sort	adhesion to and biofilm formation on ib3-1 bronchial cells by <it<stenotrophomonas maltophilia </it<isolates from cystic fibrosis patients
callnumber	QR1-502
title_auth	Adhesion to and biofilm formation on IB3-1 bronchial cells by <it<Stenotrophomonas maltophilia </it<isolates from cystic fibrosis patients
abstract	<p<Abstract</p< <p<Background</p< <p<<it<Stenotrophomonas maltophilia </it<has recently gained considerable attention as an important emerging pathogen in cystic fibrosis (CF) patients. However, the role of this microorganism in the pathophysiology of CF lung disease remains largely unexplored. In the present study for the first time we assessed the ability of <it<S. maltophilia </it<CF isolates to adhere to and form biofilm in experimental infection experiments using the CF-derived bronchial epithelial IB3-1cell line. The role of flagella on the adhesiveness of <it<S. maltophilia </it<to IB3-1 cell monolayers was also assessed by using <it<fliI </it<mutant derivative strains.</p< <p<Results</p< <p<All <it<S. maltophilia </it<CF isolates tested in the present study were able, although at different levels, to adhere to and form biofilm on IB3-1 cell monolayers. Scanning electron and confocal microscopy revealed <it<S. maltophilia </it<structures typical of biofilm formation on bronchial IB3-1 cells. The loss of flagella significantly (P < 0.001) decreased bacterial adhesiveness, if compared to that of their parental flagellated strains. <it<S. maltophilia </it<CF isolates were also able to invade IB3-1 cells, albeit at a very low level (internalization rate ranged from 0.01 to 4.94%). Pre-exposure of IB3-1 cells to <it<P. aeruginosa </it<PAO1 significantly increased <it<S. maltophilia </it<adhesiveness. Further, the presence of <it<S. maltophilia </it<negatively influenced <it<P. aeruginosa </it<PAO1 adhesiveness.</p< <p<Conclusions</p< <p<The main contribution of the present study is the finding that <it<S. maltophilia </it<is able to form biofilm on and invade CF-derived IB3-1 bronchial epithelial cells, thus posing a rationale for the persistence and the systemic spread of this opportunistic pathogen in CF patients. Experiments using <it<in vivo </it<models which more closely mimic CF pulmonary tissues will certainly be needed to validate the relevance of our results.</p<
abstractGer	<p<Abstract</p< <p<Background</p< <p<<it<Stenotrophomonas maltophilia </it<has recently gained considerable attention as an important emerging pathogen in cystic fibrosis (CF) patients. However, the role of this microorganism in the pathophysiology of CF lung disease remains largely unexplored. In the present study for the first time we assessed the ability of <it<S. maltophilia </it<CF isolates to adhere to and form biofilm in experimental infection experiments using the CF-derived bronchial epithelial IB3-1cell line. The role of flagella on the adhesiveness of <it<S. maltophilia </it<to IB3-1 cell monolayers was also assessed by using <it<fliI </it<mutant derivative strains.</p< <p<Results</p< <p<All <it<S. maltophilia </it<CF isolates tested in the present study were able, although at different levels, to adhere to and form biofilm on IB3-1 cell monolayers. Scanning electron and confocal microscopy revealed <it<S. maltophilia </it<structures typical of biofilm formation on bronchial IB3-1 cells. The loss of flagella significantly (P < 0.001) decreased bacterial adhesiveness, if compared to that of their parental flagellated strains. <it<S. maltophilia </it<CF isolates were also able to invade IB3-1 cells, albeit at a very low level (internalization rate ranged from 0.01 to 4.94%). Pre-exposure of IB3-1 cells to <it<P. aeruginosa </it<PAO1 significantly increased <it<S. maltophilia </it<adhesiveness. Further, the presence of <it<S. maltophilia </it<negatively influenced <it<P. aeruginosa </it<PAO1 adhesiveness.</p< <p<Conclusions</p< <p<The main contribution of the present study is the finding that <it<S. maltophilia </it<is able to form biofilm on and invade CF-derived IB3-1 bronchial epithelial cells, thus posing a rationale for the persistence and the systemic spread of this opportunistic pathogen in CF patients. Experiments using <it<in vivo </it<models which more closely mimic CF pulmonary tissues will certainly be needed to validate the relevance of our results.</p<
abstract_unstemmed	<p<Abstract</p< <p<Background</p< <p<<it<Stenotrophomonas maltophilia </it<has recently gained considerable attention as an important emerging pathogen in cystic fibrosis (CF) patients. However, the role of this microorganism in the pathophysiology of CF lung disease remains largely unexplored. In the present study for the first time we assessed the ability of <it<S. maltophilia </it<CF isolates to adhere to and form biofilm in experimental infection experiments using the CF-derived bronchial epithelial IB3-1cell line. The role of flagella on the adhesiveness of <it<S. maltophilia </it<to IB3-1 cell monolayers was also assessed by using <it<fliI </it<mutant derivative strains.</p< <p<Results</p< <p<All <it<S. maltophilia </it<CF isolates tested in the present study were able, although at different levels, to adhere to and form biofilm on IB3-1 cell monolayers. Scanning electron and confocal microscopy revealed <it<S. maltophilia </it<structures typical of biofilm formation on bronchial IB3-1 cells. The loss of flagella significantly (P < 0.001) decreased bacterial adhesiveness, if compared to that of their parental flagellated strains. <it<S. maltophilia </it<CF isolates were also able to invade IB3-1 cells, albeit at a very low level (internalization rate ranged from 0.01 to 4.94%). Pre-exposure of IB3-1 cells to <it<P. aeruginosa </it<PAO1 significantly increased <it<S. maltophilia </it<adhesiveness. Further, the presence of <it<S. maltophilia </it<negatively influenced <it<P. aeruginosa </it<PAO1 adhesiveness.</p< <p<Conclusions</p< <p<The main contribution of the present study is the finding that <it<S. maltophilia </it<is able to form biofilm on and invade CF-derived IB3-1 bronchial epithelial cells, thus posing a rationale for the persistence and the systemic spread of this opportunistic pathogen in CF patients. Experiments using <it<in vivo </it<models which more closely mimic CF pulmonary tissues will certainly be needed to validate the relevance of our results.</p<
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title_short	Adhesion to and biofilm formation on IB3-1 bronchial cells by <it<Stenotrophomonas maltophilia </it<isolates from cystic fibrosis patients
url	https://doi.org/10.1186/1471-2180-10-102 https://doaj.org/article/789e96b79ffc4ce2b6bfce3808eb9511 http://www.biomedcentral.com/1471-2180/10/102 https://doaj.org/toc/1471-2180
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up_date	2024-07-03T17:56:52.455Z
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However, the role of this microorganism in the pathophysiology of CF lung disease remains largely unexplored. In the present study for the first time we assessed the ability of <it<S. maltophilia </it<CF isolates to adhere to and form biofilm in experimental infection experiments using the CF-derived bronchial epithelial IB3-1cell line. The role of flagella on the adhesiveness of <it<S. maltophilia </it<to IB3-1 cell monolayers was also assessed by using <it<fliI </it<mutant derivative strains.</p< <p<Results</p< <p<All <it<S. maltophilia </it<CF isolates tested in the present study were able, although at different levels, to adhere to and form biofilm on IB3-1 cell monolayers. Scanning electron and confocal microscopy revealed <it<S. maltophilia </it<structures typical of biofilm formation on bronchial IB3-1 cells. The loss of flagella significantly (P < 0.001) decreased bacterial adhesiveness, if compared to that of their parental flagellated strains. <it<S. maltophilia </it<CF isolates were also able to invade IB3-1 cells, albeit at a very low level (internalization rate ranged from 0.01 to 4.94%). Pre-exposure of IB3-1 cells to <it<P. aeruginosa </it<PAO1 significantly increased <it<S. maltophilia </it<adhesiveness. Further, the presence of <it<S. maltophilia </it<negatively influenced <it<P. aeruginosa </it<PAO1 adhesiveness.</p< <p<Conclusions</p< <p<The main contribution of the present study is the finding that <it<S. maltophilia </it<is able to form biofilm on and invade CF-derived IB3-1 bronchial epithelial cells, thus posing a rationale for the persistence and the systemic spread of this opportunistic pathogen in CF patients. 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Adhesion to and biofilm formation on IB3-1 bronchial cells by <it<Stenotrophomonas maltophilia </it<isolates from cystic fibrosis patients

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