Rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells

Background Human rhinoviruses (RV), the most common triggers of acute asthma exacerbations, are considered not cytotoxic to the bronchial epithelium. Recent observations, however, have questioned this knowledge. The aim of this study was to evaluate the ability of RV to induce epithelial cytotoxicit...
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Autor*in:	Bossios, Apostolos [verfasserIn] Psarras, Stelios Gourgiotis, Dimitrios Skevaki, Chrysanthi L Constantopoulos, Andreas G Saxoni-Papageorgiou, Photini Papadopoulos, Nikolaos G

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2005

Schlagwörter:	Proliferate Cell Nuclear Antigen Bronchial Epithelial Cell Acute Asthma Exacerbation Epithelial Wound Healing Primary Bronchial Epithelial Cell

Anmerkung:	© Bossios et al. 2005. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (

Übergeordnetes Werk:	Enthalten in: Respiratory research - London : BioMed Central, 2001, 6(2005), 1 vom: 10. Okt.
Übergeordnetes Werk:	volume:6 ; year:2005 ; number:1 ; day:10 ; month:10

Links:	Volltext

DOI / URN:	10.1186/1465-9921-6-114

Katalog-ID:	SPR028504488

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245	1	0	\|a Rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells
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520			\|a Background Human rhinoviruses (RV), the most common triggers of acute asthma exacerbations, are considered not cytotoxic to the bronchial epithelium. Recent observations, however, have questioned this knowledge. The aim of this study was to evaluate the ability of RV to induce epithelial cytotoxicity and affect epithelial repair in-vitro. Methods Monolayers of BEAS-2B bronchial epithelial cells, seeded at different densities were exposed to RV serotypes 1b, 5, 7, 9, 14, 16. Cytotoxicity was assessed chromatometrically. Epithelial monolayers were mechanically wounded, exposed or not to RV and the repopulation of the damaged area was assessed by image analysis. Finally epithelial cell proliferation was assessed by quantitation of proliferating cell nuclear antigen (PCNA) by flow cytometry. Results RV1b, RV5, RV7, RV14 and RV16 were able to induce considerable epithelial cytotoxicity, more pronounced in less dense cultures, in a cell-density and dose-dependent manner. RV9 was not cytotoxic. Furthermore, RV infection diminished the self-repair capacity of bronchial epithelial cells and reduced cell proliferation. Conclusion RV-induced epithelial cytotoxicity may become considerable in already compromised epithelium, such as in the case of asthma. The RV-induced impairment on epithelial proliferation and self-repair capacity may contribute to the development of airway remodeling.
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700	1		\|a Psarras, Stelios \|4 aut
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700	1		\|a Saxoni-Papageorgiou, Photini \|4 aut
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allfields	10.1186/1465-9921-6-114 doi (DE-627)SPR028504488 (SPR)1465-9921-6-114-e DE-627 ger DE-627 rakwb eng Bossios, Apostolos verfasserin aut Rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Bossios et al. 2005. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Human rhinoviruses (RV), the most common triggers of acute asthma exacerbations, are considered not cytotoxic to the bronchial epithelium. Recent observations, however, have questioned this knowledge. The aim of this study was to evaluate the ability of RV to induce epithelial cytotoxicity and affect epithelial repair in-vitro. Methods Monolayers of BEAS-2B bronchial epithelial cells, seeded at different densities were exposed to RV serotypes 1b, 5, 7, 9, 14, 16. Cytotoxicity was assessed chromatometrically. Epithelial monolayers were mechanically wounded, exposed or not to RV and the repopulation of the damaged area was assessed by image analysis. Finally epithelial cell proliferation was assessed by quantitation of proliferating cell nuclear antigen (PCNA) by flow cytometry. Results RV1b, RV5, RV7, RV14 and RV16 were able to induce considerable epithelial cytotoxicity, more pronounced in less dense cultures, in a cell-density and dose-dependent manner. RV9 was not cytotoxic. Furthermore, RV infection diminished the self-repair capacity of bronchial epithelial cells and reduced cell proliferation. Conclusion RV-induced epithelial cytotoxicity may become considerable in already compromised epithelium, such as in the case of asthma. The RV-induced impairment on epithelial proliferation and self-repair capacity may contribute to the development of airway remodeling. Proliferate Cell Nuclear Antigen (dpeaa)DE-He213 Bronchial Epithelial Cell (dpeaa)DE-He213 Acute Asthma Exacerbation (dpeaa)DE-He213 Epithelial Wound Healing (dpeaa)DE-He213 Primary Bronchial Epithelial Cell (dpeaa)DE-He213 Psarras, Stelios aut Gourgiotis, Dimitrios aut Skevaki, Chrysanthi L aut Constantopoulos, Andreas G aut Saxoni-Papageorgiou, Photini aut Papadopoulos, Nikolaos G aut Enthalten in Respiratory research London : BioMed Central, 2001 6(2005), 1 vom: 10. Okt. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:6 year:2005 number:1 day:10 month:10 https://dx.doi.org/10.1186/1465-9921-6-114 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 6 2005 1 10 10
spelling	10.1186/1465-9921-6-114 doi (DE-627)SPR028504488 (SPR)1465-9921-6-114-e DE-627 ger DE-627 rakwb eng Bossios, Apostolos verfasserin aut Rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Bossios et al. 2005. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Human rhinoviruses (RV), the most common triggers of acute asthma exacerbations, are considered not cytotoxic to the bronchial epithelium. Recent observations, however, have questioned this knowledge. The aim of this study was to evaluate the ability of RV to induce epithelial cytotoxicity and affect epithelial repair in-vitro. Methods Monolayers of BEAS-2B bronchial epithelial cells, seeded at different densities were exposed to RV serotypes 1b, 5, 7, 9, 14, 16. Cytotoxicity was assessed chromatometrically. Epithelial monolayers were mechanically wounded, exposed or not to RV and the repopulation of the damaged area was assessed by image analysis. Finally epithelial cell proliferation was assessed by quantitation of proliferating cell nuclear antigen (PCNA) by flow cytometry. Results RV1b, RV5, RV7, RV14 and RV16 were able to induce considerable epithelial cytotoxicity, more pronounced in less dense cultures, in a cell-density and dose-dependent manner. RV9 was not cytotoxic. Furthermore, RV infection diminished the self-repair capacity of bronchial epithelial cells and reduced cell proliferation. Conclusion RV-induced epithelial cytotoxicity may become considerable in already compromised epithelium, such as in the case of asthma. The RV-induced impairment on epithelial proliferation and self-repair capacity may contribute to the development of airway remodeling. Proliferate Cell Nuclear Antigen (dpeaa)DE-He213 Bronchial Epithelial Cell (dpeaa)DE-He213 Acute Asthma Exacerbation (dpeaa)DE-He213 Epithelial Wound Healing (dpeaa)DE-He213 Primary Bronchial Epithelial Cell (dpeaa)DE-He213 Psarras, Stelios aut Gourgiotis, Dimitrios aut Skevaki, Chrysanthi L aut Constantopoulos, Andreas G aut Saxoni-Papageorgiou, Photini aut Papadopoulos, Nikolaos G aut Enthalten in Respiratory research London : BioMed Central, 2001 6(2005), 1 vom: 10. Okt. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:6 year:2005 number:1 day:10 month:10 https://dx.doi.org/10.1186/1465-9921-6-114 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 6 2005 1 10 10
allfields_unstemmed	10.1186/1465-9921-6-114 doi (DE-627)SPR028504488 (SPR)1465-9921-6-114-e DE-627 ger DE-627 rakwb eng Bossios, Apostolos verfasserin aut Rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Bossios et al. 2005. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Human rhinoviruses (RV), the most common triggers of acute asthma exacerbations, are considered not cytotoxic to the bronchial epithelium. Recent observations, however, have questioned this knowledge. The aim of this study was to evaluate the ability of RV to induce epithelial cytotoxicity and affect epithelial repair in-vitro. Methods Monolayers of BEAS-2B bronchial epithelial cells, seeded at different densities were exposed to RV serotypes 1b, 5, 7, 9, 14, 16. Cytotoxicity was assessed chromatometrically. Epithelial monolayers were mechanically wounded, exposed or not to RV and the repopulation of the damaged area was assessed by image analysis. Finally epithelial cell proliferation was assessed by quantitation of proliferating cell nuclear antigen (PCNA) by flow cytometry. Results RV1b, RV5, RV7, RV14 and RV16 were able to induce considerable epithelial cytotoxicity, more pronounced in less dense cultures, in a cell-density and dose-dependent manner. RV9 was not cytotoxic. Furthermore, RV infection diminished the self-repair capacity of bronchial epithelial cells and reduced cell proliferation. Conclusion RV-induced epithelial cytotoxicity may become considerable in already compromised epithelium, such as in the case of asthma. The RV-induced impairment on epithelial proliferation and self-repair capacity may contribute to the development of airway remodeling. Proliferate Cell Nuclear Antigen (dpeaa)DE-He213 Bronchial Epithelial Cell (dpeaa)DE-He213 Acute Asthma Exacerbation (dpeaa)DE-He213 Epithelial Wound Healing (dpeaa)DE-He213 Primary Bronchial Epithelial Cell (dpeaa)DE-He213 Psarras, Stelios aut Gourgiotis, Dimitrios aut Skevaki, Chrysanthi L aut Constantopoulos, Andreas G aut Saxoni-Papageorgiou, Photini aut Papadopoulos, Nikolaos G aut Enthalten in Respiratory research London : BioMed Central, 2001 6(2005), 1 vom: 10. Okt. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:6 year:2005 number:1 day:10 month:10 https://dx.doi.org/10.1186/1465-9921-6-114 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 6 2005 1 10 10
allfieldsGer	10.1186/1465-9921-6-114 doi (DE-627)SPR028504488 (SPR)1465-9921-6-114-e DE-627 ger DE-627 rakwb eng Bossios, Apostolos verfasserin aut Rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Bossios et al. 2005. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Human rhinoviruses (RV), the most common triggers of acute asthma exacerbations, are considered not cytotoxic to the bronchial epithelium. Recent observations, however, have questioned this knowledge. The aim of this study was to evaluate the ability of RV to induce epithelial cytotoxicity and affect epithelial repair in-vitro. Methods Monolayers of BEAS-2B bronchial epithelial cells, seeded at different densities were exposed to RV serotypes 1b, 5, 7, 9, 14, 16. Cytotoxicity was assessed chromatometrically. Epithelial monolayers were mechanically wounded, exposed or not to RV and the repopulation of the damaged area was assessed by image analysis. Finally epithelial cell proliferation was assessed by quantitation of proliferating cell nuclear antigen (PCNA) by flow cytometry. Results RV1b, RV5, RV7, RV14 and RV16 were able to induce considerable epithelial cytotoxicity, more pronounced in less dense cultures, in a cell-density and dose-dependent manner. RV9 was not cytotoxic. Furthermore, RV infection diminished the self-repair capacity of bronchial epithelial cells and reduced cell proliferation. Conclusion RV-induced epithelial cytotoxicity may become considerable in already compromised epithelium, such as in the case of asthma. The RV-induced impairment on epithelial proliferation and self-repair capacity may contribute to the development of airway remodeling. Proliferate Cell Nuclear Antigen (dpeaa)DE-He213 Bronchial Epithelial Cell (dpeaa)DE-He213 Acute Asthma Exacerbation (dpeaa)DE-He213 Epithelial Wound Healing (dpeaa)DE-He213 Primary Bronchial Epithelial Cell (dpeaa)DE-He213 Psarras, Stelios aut Gourgiotis, Dimitrios aut Skevaki, Chrysanthi L aut Constantopoulos, Andreas G aut Saxoni-Papageorgiou, Photini aut Papadopoulos, Nikolaos G aut Enthalten in Respiratory research London : BioMed Central, 2001 6(2005), 1 vom: 10. Okt. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:6 year:2005 number:1 day:10 month:10 https://dx.doi.org/10.1186/1465-9921-6-114 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 6 2005 1 10 10
allfieldsSound	10.1186/1465-9921-6-114 doi (DE-627)SPR028504488 (SPR)1465-9921-6-114-e DE-627 ger DE-627 rakwb eng Bossios, Apostolos verfasserin aut Rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Bossios et al. 2005. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Human rhinoviruses (RV), the most common triggers of acute asthma exacerbations, are considered not cytotoxic to the bronchial epithelium. Recent observations, however, have questioned this knowledge. The aim of this study was to evaluate the ability of RV to induce epithelial cytotoxicity and affect epithelial repair in-vitro. Methods Monolayers of BEAS-2B bronchial epithelial cells, seeded at different densities were exposed to RV serotypes 1b, 5, 7, 9, 14, 16. Cytotoxicity was assessed chromatometrically. Epithelial monolayers were mechanically wounded, exposed or not to RV and the repopulation of the damaged area was assessed by image analysis. Finally epithelial cell proliferation was assessed by quantitation of proliferating cell nuclear antigen (PCNA) by flow cytometry. Results RV1b, RV5, RV7, RV14 and RV16 were able to induce considerable epithelial cytotoxicity, more pronounced in less dense cultures, in a cell-density and dose-dependent manner. RV9 was not cytotoxic. Furthermore, RV infection diminished the self-repair capacity of bronchial epithelial cells and reduced cell proliferation. Conclusion RV-induced epithelial cytotoxicity may become considerable in already compromised epithelium, such as in the case of asthma. The RV-induced impairment on epithelial proliferation and self-repair capacity may contribute to the development of airway remodeling. Proliferate Cell Nuclear Antigen (dpeaa)DE-He213 Bronchial Epithelial Cell (dpeaa)DE-He213 Acute Asthma Exacerbation (dpeaa)DE-He213 Epithelial Wound Healing (dpeaa)DE-He213 Primary Bronchial Epithelial Cell (dpeaa)DE-He213 Psarras, Stelios aut Gourgiotis, Dimitrios aut Skevaki, Chrysanthi L aut Constantopoulos, Andreas G aut Saxoni-Papageorgiou, Photini aut Papadopoulos, Nikolaos G aut Enthalten in Respiratory research London : BioMed Central, 2001 6(2005), 1 vom: 10. Okt. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:6 year:2005 number:1 day:10 month:10 https://dx.doi.org/10.1186/1465-9921-6-114 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 6 2005 1 10 10
language	English
source	Enthalten in Respiratory research 6(2005), 1 vom: 10. Okt. volume:6 year:2005 number:1 day:10 month:10
sourceStr	Enthalten in Respiratory research 6(2005), 1 vom: 10. Okt. volume:6 year:2005 number:1 day:10 month:10
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Proliferate Cell Nuclear Antigen Bronchial Epithelial Cell Acute Asthma Exacerbation Epithelial Wound Healing Primary Bronchial Epithelial Cell
isfreeaccess_bool	true
container_title	Respiratory research
authorswithroles_txt_mv	Bossios, Apostolos @@aut@@ Psarras, Stelios @@aut@@ Gourgiotis, Dimitrios @@aut@@ Skevaki, Chrysanthi L @@aut@@ Constantopoulos, Andreas G @@aut@@ Saxoni-Papageorgiou, Photini @@aut@@ Papadopoulos, Nikolaos G @@aut@@
publishDateDaySort_date	2005-10-10T00:00:00Z
hierarchy_top_id	326646485
id	SPR028504488
language_de	englisch
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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Human rhinoviruses (RV), the most common triggers of acute asthma exacerbations, are considered not cytotoxic to the bronchial epithelium. Recent observations, however, have questioned this knowledge. The aim of this study was to evaluate the ability of RV to induce epithelial cytotoxicity and affect epithelial repair in-vitro. Methods Monolayers of BEAS-2B bronchial epithelial cells, seeded at different densities were exposed to RV serotypes 1b, 5, 7, 9, 14, 16. Cytotoxicity was assessed chromatometrically. Epithelial monolayers were mechanically wounded, exposed or not to RV and the repopulation of the damaged area was assessed by image analysis. Finally epithelial cell proliferation was assessed by quantitation of proliferating cell nuclear antigen (PCNA) by flow cytometry. Results RV1b, RV5, RV7, RV14 and RV16 were able to induce considerable epithelial cytotoxicity, more pronounced in less dense cultures, in a cell-density and dose-dependent manner. RV9 was not cytotoxic. Furthermore, RV infection diminished the self-repair capacity of bronchial epithelial cells and reduced cell proliferation. Conclusion RV-induced epithelial cytotoxicity may become considerable in already compromised epithelium, such as in the case of asthma. 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author	Bossios, Apostolos
spellingShingle	Bossios, Apostolos misc Proliferate Cell Nuclear Antigen misc Bronchial Epithelial Cell misc Acute Asthma Exacerbation misc Epithelial Wound Healing misc Primary Bronchial Epithelial Cell Rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells
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topic_title	Rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells Proliferate Cell Nuclear Antigen (dpeaa)DE-He213 Bronchial Epithelial Cell (dpeaa)DE-He213 Acute Asthma Exacerbation (dpeaa)DE-He213 Epithelial Wound Healing (dpeaa)DE-He213 Primary Bronchial Epithelial Cell (dpeaa)DE-He213
topic	misc Proliferate Cell Nuclear Antigen misc Bronchial Epithelial Cell misc Acute Asthma Exacerbation misc Epithelial Wound Healing misc Primary Bronchial Epithelial Cell
topic_unstemmed	misc Proliferate Cell Nuclear Antigen misc Bronchial Epithelial Cell misc Acute Asthma Exacerbation misc Epithelial Wound Healing misc Primary Bronchial Epithelial Cell
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title	Rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells
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title_full	Rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells
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author_browse	Bossios, Apostolos Psarras, Stelios Gourgiotis, Dimitrios Skevaki, Chrysanthi L Constantopoulos, Andreas G Saxoni-Papageorgiou, Photini Papadopoulos, Nikolaos G
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title_sort	rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells
title_auth	Rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells
abstract	Background Human rhinoviruses (RV), the most common triggers of acute asthma exacerbations, are considered not cytotoxic to the bronchial epithelium. Recent observations, however, have questioned this knowledge. The aim of this study was to evaluate the ability of RV to induce epithelial cytotoxicity and affect epithelial repair in-vitro. Methods Monolayers of BEAS-2B bronchial epithelial cells, seeded at different densities were exposed to RV serotypes 1b, 5, 7, 9, 14, 16. Cytotoxicity was assessed chromatometrically. Epithelial monolayers were mechanically wounded, exposed or not to RV and the repopulation of the damaged area was assessed by image analysis. Finally epithelial cell proliferation was assessed by quantitation of proliferating cell nuclear antigen (PCNA) by flow cytometry. Results RV1b, RV5, RV7, RV14 and RV16 were able to induce considerable epithelial cytotoxicity, more pronounced in less dense cultures, in a cell-density and dose-dependent manner. RV9 was not cytotoxic. Furthermore, RV infection diminished the self-repair capacity of bronchial epithelial cells and reduced cell proliferation. Conclusion RV-induced epithelial cytotoxicity may become considerable in already compromised epithelium, such as in the case of asthma. The RV-induced impairment on epithelial proliferation and self-repair capacity may contribute to the development of airway remodeling. © Bossios et al. 2005. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstractGer	Background Human rhinoviruses (RV), the most common triggers of acute asthma exacerbations, are considered not cytotoxic to the bronchial epithelium. Recent observations, however, have questioned this knowledge. The aim of this study was to evaluate the ability of RV to induce epithelial cytotoxicity and affect epithelial repair in-vitro. Methods Monolayers of BEAS-2B bronchial epithelial cells, seeded at different densities were exposed to RV serotypes 1b, 5, 7, 9, 14, 16. Cytotoxicity was assessed chromatometrically. Epithelial monolayers were mechanically wounded, exposed or not to RV and the repopulation of the damaged area was assessed by image analysis. Finally epithelial cell proliferation was assessed by quantitation of proliferating cell nuclear antigen (PCNA) by flow cytometry. Results RV1b, RV5, RV7, RV14 and RV16 were able to induce considerable epithelial cytotoxicity, more pronounced in less dense cultures, in a cell-density and dose-dependent manner. RV9 was not cytotoxic. Furthermore, RV infection diminished the self-repair capacity of bronchial epithelial cells and reduced cell proliferation. Conclusion RV-induced epithelial cytotoxicity may become considerable in already compromised epithelium, such as in the case of asthma. The RV-induced impairment on epithelial proliferation and self-repair capacity may contribute to the development of airway remodeling. © Bossios et al. 2005. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstract_unstemmed	Background Human rhinoviruses (RV), the most common triggers of acute asthma exacerbations, are considered not cytotoxic to the bronchial epithelium. Recent observations, however, have questioned this knowledge. The aim of this study was to evaluate the ability of RV to induce epithelial cytotoxicity and affect epithelial repair in-vitro. Methods Monolayers of BEAS-2B bronchial epithelial cells, seeded at different densities were exposed to RV serotypes 1b, 5, 7, 9, 14, 16. Cytotoxicity was assessed chromatometrically. Epithelial monolayers were mechanically wounded, exposed or not to RV and the repopulation of the damaged area was assessed by image analysis. Finally epithelial cell proliferation was assessed by quantitation of proliferating cell nuclear antigen (PCNA) by flow cytometry. Results RV1b, RV5, RV7, RV14 and RV16 were able to induce considerable epithelial cytotoxicity, more pronounced in less dense cultures, in a cell-density and dose-dependent manner. RV9 was not cytotoxic. Furthermore, RV infection diminished the self-repair capacity of bronchial epithelial cells and reduced cell proliferation. Conclusion RV-induced epithelial cytotoxicity may become considerable in already compromised epithelium, such as in the case of asthma. The RV-induced impairment on epithelial proliferation and self-repair capacity may contribute to the development of airway remodeling. © Bossios et al. 2005. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
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title_short	Rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells
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Rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells

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