Interleukin-6 contributes to inflammation and remodeling in a model of adenosine mediated lung injury.

<h4>Background</h4>Chronic lung diseases are the third leading cause of death in the United States due in part to an incomplete understanding of pathways that govern the progressive tissue remodeling that occurs in these disorders. Adenosine is elevated in the lungs of animal models and...

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Autores principales:	Mesias Pedroza, Daniel J Schneider, Harry Karmouty-Quintana, Julie Coote, Stevan Shaw, Rebecca Corrigan, Jose G Molina, Joseph L Alcorn, David Galas, Richard Gelinas, Michael R Blackburn
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/55b1329ceccf4e169ad2b50505e6c82d
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spelling	oai:doaj.org-article:55b1329ceccf4e169ad2b50505e6c82d2021-11-18T06:49:27ZInterleukin-6 contributes to inflammation and remodeling in a model of adenosine mediated lung injury.1932-620310.1371/journal.pone.0022667https://doaj.org/article/55b1329ceccf4e169ad2b50505e6c82d2011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21799929/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Chronic lung diseases are the third leading cause of death in the United States due in part to an incomplete understanding of pathways that govern the progressive tissue remodeling that occurs in these disorders. Adenosine is elevated in the lungs of animal models and humans with chronic lung disease where it promotes air-space destruction and fibrosis. Adenosine signaling increases the production of the pro-fibrotic cytokine interleukin-6 (IL-6). Based on these observations, we hypothesized that IL-6 signaling contributes to tissue destruction and remodeling in a model of chronic lung disease where adenosine levels are elevated.<h4>Methodology/principal findings</h4>We tested this hypothesis by neutralizing or genetically removing IL-6 in adenosine deaminase (ADA)-deficient mice that develop adenosine dependent pulmonary inflammation and remodeling. Results demonstrated that both pharmacologic blockade and genetic removal of IL-6 attenuated pulmonary inflammation, remodeling and fibrosis in this model. The pursuit of mechanisms involved revealed adenosine and IL-6 dependent activation of STAT-3 in airway epithelial cells.<h4>Conclusions/significance</h4>These findings demonstrate that adenosine enhances IL-6 signaling pathways to promote aspects of chronic lung disease. This suggests that blocking IL-6 signaling during chronic stages of disease may provide benefit in halting remodeling processes such as fibrosis and air-space destruction.Mesias PedrozaDaniel J SchneiderHarry Karmouty-QuintanaJulie CooteStevan ShawRebecca CorriganJose G MolinaJoseph L AlcornDavid GalasRichard GelinasMichael R BlackburnPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 7, p e22667 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Mesias Pedroza Daniel J Schneider Harry Karmouty-Quintana Julie Coote Stevan Shaw Rebecca Corrigan Jose G Molina Joseph L Alcorn David Galas Richard Gelinas Michael R Blackburn Interleukin-6 contributes to inflammation and remodeling in a model of adenosine mediated lung injury.
description	<h4>Background</h4>Chronic lung diseases are the third leading cause of death in the United States due in part to an incomplete understanding of pathways that govern the progressive tissue remodeling that occurs in these disorders. Adenosine is elevated in the lungs of animal models and humans with chronic lung disease where it promotes air-space destruction and fibrosis. Adenosine signaling increases the production of the pro-fibrotic cytokine interleukin-6 (IL-6). Based on these observations, we hypothesized that IL-6 signaling contributes to tissue destruction and remodeling in a model of chronic lung disease where adenosine levels are elevated.<h4>Methodology/principal findings</h4>We tested this hypothesis by neutralizing or genetically removing IL-6 in adenosine deaminase (ADA)-deficient mice that develop adenosine dependent pulmonary inflammation and remodeling. Results demonstrated that both pharmacologic blockade and genetic removal of IL-6 attenuated pulmonary inflammation, remodeling and fibrosis in this model. The pursuit of mechanisms involved revealed adenosine and IL-6 dependent activation of STAT-3 in airway epithelial cells.<h4>Conclusions/significance</h4>These findings demonstrate that adenosine enhances IL-6 signaling pathways to promote aspects of chronic lung disease. This suggests that blocking IL-6 signaling during chronic stages of disease may provide benefit in halting remodeling processes such as fibrosis and air-space destruction.
format	article
author	Mesias Pedroza Daniel J Schneider Harry Karmouty-Quintana Julie Coote Stevan Shaw Rebecca Corrigan Jose G Molina Joseph L Alcorn David Galas Richard Gelinas Michael R Blackburn
author_facet	Mesias Pedroza Daniel J Schneider Harry Karmouty-Quintana Julie Coote Stevan Shaw Rebecca Corrigan Jose G Molina Joseph L Alcorn David Galas Richard Gelinas Michael R Blackburn
author_sort	Mesias Pedroza
title	Interleukin-6 contributes to inflammation and remodeling in a model of adenosine mediated lung injury.
title_short	Interleukin-6 contributes to inflammation and remodeling in a model of adenosine mediated lung injury.
title_full	Interleukin-6 contributes to inflammation and remodeling in a model of adenosine mediated lung injury.
title_fullStr	Interleukin-6 contributes to inflammation and remodeling in a model of adenosine mediated lung injury.
title_full_unstemmed	Interleukin-6 contributes to inflammation and remodeling in a model of adenosine mediated lung injury.
title_sort	interleukin-6 contributes to inflammation and remodeling in a model of adenosine mediated lung injury.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/55b1329ceccf4e169ad2b50505e6c82d
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Interleukin-6 contributes to inflammation and remodeling in a model of adenosine mediated lung injury.

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