Convergent sets of data from in vivo and in vitro methods point to an active role of Hsp60 in chronic obstructive pulmonary disease pathogenesis.

<h4>Background</h4>It is increasingly clear that some heat shock proteins (Hsps) play a role in inflammation. Here, we report results showing participation of Hsp60 in the pathogenesis of chronic obstructive pulmonary diseases (COPD), as indicated by data from both in vivo and in vitro a...

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Autores principales: Francesco Cappello, Gaetano Caramori, Claudia Campanella, Chiara Vicari, Isabella Gnemmi, Andrea Zanini, Antonio Spanevello, Armando Capelli, Giampiero La Rocca, Rita Anzalone, Fabio Bucchieri, Silvestro Ennio D'Anna, Fabio L M Ricciardolo, Paola Brun, Bruno Balbi, Mauro Carone, Giovanni Zummo, Everly Conway de Macario, Alberto J L Macario, Antonino Di Stefano
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spelling oai:doaj.org-article:17adeac62af342d3ae37bd8812d2dade2021-11-18T07:33:30ZConvergent sets of data from in vivo and in vitro methods point to an active role of Hsp60 in chronic obstructive pulmonary disease pathogenesis.1932-620310.1371/journal.pone.0028200https://doaj.org/article/17adeac62af342d3ae37bd8812d2dade2011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22140545/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>It is increasingly clear that some heat shock proteins (Hsps) play a role in inflammation. Here, we report results showing participation of Hsp60 in the pathogenesis of chronic obstructive pulmonary diseases (COPD), as indicated by data from both in vivo and in vitro analyses.<h4>Methods and results</h4>Bronchial biopsies from patients with stable COPD, smoker controls with normal lung function, and non-smoker controls were studied. We quantified by immunohistochemistry levels of Hsp10, Hsp27, Hsp40, Hsp60, Hsp70, Hsp90, and HSF-1, along with levels of inflammatory markers. Hsp10, Hsp40, and Hsp60 were increased during progression of disease. We found also a positive correlation between the number of neutrophils and Hsp60 levels. Double-immunostaining showed that Hsp60-positive neutrophils were significantly increased in COPD patients. We then investigated in vitro the effect on Hsp60 expression in bronchial epithelial cells (16HBE) caused by oxidative stress, a hallmark of COPD mucosa, which we induced with H₂O₂. This stressor determined increased levels of Hsp60 through a gene up-regulation mechanism involving NFkB-p65. Release of Hsp60 in the extracellular medium by the bronchial epithelial cells was also increased after H₂O₂ treatment in the absence of cell death.<h4>Conclusions</h4>This is the first report clearly pointing to participation of Hsps, particularly Hsp60, in COPD pathogenesis. Hsp60 induction by NFkB-p65 and its release by epithelial cells after oxidative stress can have a role in maintaining inflammation, e.g., by stimulating neutrophils activity. The data open new scenarios that might help in designing efficacious anti-inflammatory therapies centered on Hsp60 and applicable to COPD.Francesco CappelloGaetano CaramoriClaudia CampanellaChiara VicariIsabella GnemmiAndrea ZaniniAntonio SpanevelloArmando CapelliGiampiero La RoccaRita AnzaloneFabio BucchieriSilvestro Ennio D'AnnaFabio L M RicciardoloPaola BrunBruno BalbiMauro CaroneGiovanni ZummoEverly Conway de MacarioAlberto J L MacarioAntonino Di StefanoPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 11, p e28200 (2011)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Francesco Cappello
Gaetano Caramori
Claudia Campanella
Chiara Vicari
Isabella Gnemmi
Andrea Zanini
Antonio Spanevello
Armando Capelli
Giampiero La Rocca
Rita Anzalone
Fabio Bucchieri
Silvestro Ennio D'Anna
Fabio L M Ricciardolo
Paola Brun
Bruno Balbi
Mauro Carone
Giovanni Zummo
Everly Conway de Macario
Alberto J L Macario
Antonino Di Stefano
Convergent sets of data from in vivo and in vitro methods point to an active role of Hsp60 in chronic obstructive pulmonary disease pathogenesis.
description <h4>Background</h4>It is increasingly clear that some heat shock proteins (Hsps) play a role in inflammation. Here, we report results showing participation of Hsp60 in the pathogenesis of chronic obstructive pulmonary diseases (COPD), as indicated by data from both in vivo and in vitro analyses.<h4>Methods and results</h4>Bronchial biopsies from patients with stable COPD, smoker controls with normal lung function, and non-smoker controls were studied. We quantified by immunohistochemistry levels of Hsp10, Hsp27, Hsp40, Hsp60, Hsp70, Hsp90, and HSF-1, along with levels of inflammatory markers. Hsp10, Hsp40, and Hsp60 were increased during progression of disease. We found also a positive correlation between the number of neutrophils and Hsp60 levels. Double-immunostaining showed that Hsp60-positive neutrophils were significantly increased in COPD patients. We then investigated in vitro the effect on Hsp60 expression in bronchial epithelial cells (16HBE) caused by oxidative stress, a hallmark of COPD mucosa, which we induced with H₂O₂. This stressor determined increased levels of Hsp60 through a gene up-regulation mechanism involving NFkB-p65. Release of Hsp60 in the extracellular medium by the bronchial epithelial cells was also increased after H₂O₂ treatment in the absence of cell death.<h4>Conclusions</h4>This is the first report clearly pointing to participation of Hsps, particularly Hsp60, in COPD pathogenesis. Hsp60 induction by NFkB-p65 and its release by epithelial cells after oxidative stress can have a role in maintaining inflammation, e.g., by stimulating neutrophils activity. The data open new scenarios that might help in designing efficacious anti-inflammatory therapies centered on Hsp60 and applicable to COPD.
format article
author Francesco Cappello
Gaetano Caramori
Claudia Campanella
Chiara Vicari
Isabella Gnemmi
Andrea Zanini
Antonio Spanevello
Armando Capelli
Giampiero La Rocca
Rita Anzalone
Fabio Bucchieri
Silvestro Ennio D'Anna
Fabio L M Ricciardolo
Paola Brun
Bruno Balbi
Mauro Carone
Giovanni Zummo
Everly Conway de Macario
Alberto J L Macario
Antonino Di Stefano
author_facet Francesco Cappello
Gaetano Caramori
Claudia Campanella
Chiara Vicari
Isabella Gnemmi
Andrea Zanini
Antonio Spanevello
Armando Capelli
Giampiero La Rocca
Rita Anzalone
Fabio Bucchieri
Silvestro Ennio D'Anna
Fabio L M Ricciardolo
Paola Brun
Bruno Balbi
Mauro Carone
Giovanni Zummo
Everly Conway de Macario
Alberto J L Macario
Antonino Di Stefano
author_sort Francesco Cappello
title Convergent sets of data from in vivo and in vitro methods point to an active role of Hsp60 in chronic obstructive pulmonary disease pathogenesis.
title_short Convergent sets of data from in vivo and in vitro methods point to an active role of Hsp60 in chronic obstructive pulmonary disease pathogenesis.
title_full Convergent sets of data from in vivo and in vitro methods point to an active role of Hsp60 in chronic obstructive pulmonary disease pathogenesis.
title_fullStr Convergent sets of data from in vivo and in vitro methods point to an active role of Hsp60 in chronic obstructive pulmonary disease pathogenesis.
title_full_unstemmed Convergent sets of data from in vivo and in vitro methods point to an active role of Hsp60 in chronic obstructive pulmonary disease pathogenesis.
title_sort convergent sets of data from in vivo and in vitro methods point to an active role of hsp60 in chronic obstructive pulmonary disease pathogenesis.
publisher Public Library of Science (PLoS)
publishDate 2011
url https://doaj.org/article/17adeac62af342d3ae37bd8812d2dade
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