Anti-inflammatory preconditioning by agonists of adenosine A1 receptor.

<h4>Background</h4>Adenosine levels rise during inflammation and modulate inflammatory responses by engaging with four different G protein-coupled receptors. It is suggested that adenosine exhibits pro-inflammatory effects through its A(1) receptor (A(1)R), and anti-inflammatory effects...

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Autores principales:	Sigal Nakav, Cidio Chaimovitz, Yuval Sufaro, Eli C Lewis, Gad Shaked, David Czeiger, Moshe Zlotnik, Amos Douvdevani
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2008
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/e38ac4e55bc546fd9e0a1d3293f201ef
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spelling	oai:doaj.org-article:e38ac4e55bc546fd9e0a1d3293f201ef2021-11-25T06:12:37ZAnti-inflammatory preconditioning by agonists of adenosine A1 receptor.1932-620310.1371/journal.pone.0002107https://doaj.org/article/e38ac4e55bc546fd9e0a1d3293f201ef2008-05-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/18461129/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Adenosine levels rise during inflammation and modulate inflammatory responses by engaging with four different G protein-coupled receptors. It is suggested that adenosine exhibits pro-inflammatory effects through its A(1) receptor (A(1)R), and anti-inflammatory effects through A(2A) receptor (A(2A)R). Therefore, understanding of the mechanisms that govern adenosine receptor regulation may advance treatment of various inflammatory disorders. We previously reported that peak A(1)R expression during leukocyte recruitment, is followed by a peak in A(2A)R during inflammation resolution.<h4>Principal findings</h4>Here, we examined whether A(1)R activation sequentially induces A(2A)R expression and by this reverses inflammation. The effect of adenosine on A(1)R mediated A(2A)R expression was examined in peritoneal macrophages (PMPhi) and primary peritoneal mesothelial cells (PMC) in vitro. Induction of A(2A)R was inhibited by pertussis toxin (PTX) and partly dependent on A(2A)R stimulation. Administration of A(1)R agonists to healthy mice reduced A(1)R expression and induced A(2A)R production in PMC. Mice that were preconditioned with A(1)R agonists 24 hours before E. coli inoculation exhibited decreased TNFalpha and IL-6 sera levels and reduced leukocytes recruitment. Preconditioning was blocked by pretreatment with A(1)R antagonist, as well as, or by late treatment with A(2A)R antagonist, and was absent in A(2A)R(-/-) mice.<h4>Conclusions</h4>Our data suggest that preconditioning by an A(1)R-agonist promotes the resolution of inflammation by inducing the production of A(2A)R. Future implications may include early treatment during inflammatory disorders or pretreatment before anticipated high risk inflammatory events, such as invasive surgery and organ transplantation.Sigal NakavCidio ChaimovitzYuval SufaroEli C LewisGad ShakedDavid CzeigerMoshe ZlotnikAmos DouvdevaniPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 3, Iss 5, p e2107 (2008)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Sigal Nakav Cidio Chaimovitz Yuval Sufaro Eli C Lewis Gad Shaked David Czeiger Moshe Zlotnik Amos Douvdevani Anti-inflammatory preconditioning by agonists of adenosine A1 receptor.
description	<h4>Background</h4>Adenosine levels rise during inflammation and modulate inflammatory responses by engaging with four different G protein-coupled receptors. It is suggested that adenosine exhibits pro-inflammatory effects through its A(1) receptor (A(1)R), and anti-inflammatory effects through A(2A) receptor (A(2A)R). Therefore, understanding of the mechanisms that govern adenosine receptor regulation may advance treatment of various inflammatory disorders. We previously reported that peak A(1)R expression during leukocyte recruitment, is followed by a peak in A(2A)R during inflammation resolution.<h4>Principal findings</h4>Here, we examined whether A(1)R activation sequentially induces A(2A)R expression and by this reverses inflammation. The effect of adenosine on A(1)R mediated A(2A)R expression was examined in peritoneal macrophages (PMPhi) and primary peritoneal mesothelial cells (PMC) in vitro. Induction of A(2A)R was inhibited by pertussis toxin (PTX) and partly dependent on A(2A)R stimulation. Administration of A(1)R agonists to healthy mice reduced A(1)R expression and induced A(2A)R production in PMC. Mice that were preconditioned with A(1)R agonists 24 hours before E. coli inoculation exhibited decreased TNFalpha and IL-6 sera levels and reduced leukocytes recruitment. Preconditioning was blocked by pretreatment with A(1)R antagonist, as well as, or by late treatment with A(2A)R antagonist, and was absent in A(2A)R(-/-) mice.<h4>Conclusions</h4>Our data suggest that preconditioning by an A(1)R-agonist promotes the resolution of inflammation by inducing the production of A(2A)R. Future implications may include early treatment during inflammatory disorders or pretreatment before anticipated high risk inflammatory events, such as invasive surgery and organ transplantation.
format	article
author	Sigal Nakav Cidio Chaimovitz Yuval Sufaro Eli C Lewis Gad Shaked David Czeiger Moshe Zlotnik Amos Douvdevani
author_facet	Sigal Nakav Cidio Chaimovitz Yuval Sufaro Eli C Lewis Gad Shaked David Czeiger Moshe Zlotnik Amos Douvdevani
author_sort	Sigal Nakav
title	Anti-inflammatory preconditioning by agonists of adenosine A1 receptor.
title_short	Anti-inflammatory preconditioning by agonists of adenosine A1 receptor.
title_full	Anti-inflammatory preconditioning by agonists of adenosine A1 receptor.
title_fullStr	Anti-inflammatory preconditioning by agonists of adenosine A1 receptor.
title_full_unstemmed	Anti-inflammatory preconditioning by agonists of adenosine A1 receptor.
title_sort	anti-inflammatory preconditioning by agonists of adenosine a1 receptor.
publisher	Public Library of Science (PLoS)
publishDate	2008
url	https://doaj.org/article/e38ac4e55bc546fd9e0a1d3293f201ef
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Anti-inflammatory preconditioning by agonists of adenosine A1 receptor.

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