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An anti-interleukin-2 receptor drug attenuates thelper 1 lymphocytes-mediated inflammation in an acute model of endotoxin-induced uveitis
dc.contributor.author | Mérida, S. | |
dc.contributor.author | Sancho Tello, M. | |
dc.contributor.author | Navea, A. | |
dc.contributor.author | Almansa, Inmaculada | |
dc.contributor.author | Muriach Saurí, María | |
dc.contributor.author | Bosch Morell, F. | |
dc.date.accessioned | 2015-06-10T18:56:44Z | |
dc.date.available | 2015-06-10T18:56:44Z | |
dc.date.issued | 2014 | |
dc.identifier.citation | Mérida S, Sancho-Tello M, Navea A, Almansa I, Muriach M, Bosch-Morell F (2014) An Anti-Interleukin-2 Receptor Drug Attenuates T- Helper 1 Lymphocytes-Mediated Inflammation in an Acute Model of Endotoxin-Induced Uveitis. PLoS ONE 9(3): e90216. doi:10.1371/journal.pone.0090216 | ca_CA |
dc.identifier.issn | 1932-6203 | |
dc.identifier.uri | http://hdl.handle.net/10234/123083 | |
dc.description.abstract | The aim of the present study was to evaluate the anti-inflammatory efficacy of Daclizumab, an anti-interleukin-2 receptor drug, in an experimental uveitis model upon a subcutaneous injection of lipopolysaccharide into Lewis rats, a valuable model for ocular acute inflammatory processes. The integrity of the blood-aqueous barrier was assessed 24 h after endotoxin-induced uveitis by evaluating two parameters: cell count and protein concentration in aqueous humors. The histopathology of all the ocular structures (cornea, lens, sclera, choroid, retina, uvea, and anterior and posterior chambers) was also considered. Enzyme-linked immunosorbent assays of the aqueous humor samples were performed to quantify the levels of the different chemokine and cytokine proteins. Similarly, a biochemical analysis of oxidative stress-related markers was also assessed. The inflammation observed in the anterior chamber of the eyes when Daclizumab was administered with endotoxin was largely prevented since the aqueous humor protein concentration substantially lowered concomitantly with a significant reduction in the uveal and vitreous histopathological grading. Th1 lymphocytes-related cytokines, such as Interleukin-2 and Interferon-c, also significantly reduced with related anti-oxidant systems recovery. Daclizumab treatment in endotoxin-induced uveitis reduced Th1 lymphocytes-related cytokines, such as Interleukin-2 and Interferon gamma, by about 60–70% and presented a preventive role in endotoxin-induced oxidative stress. This antioxidant protective effect of Daclizumab may be related to several of the observed Daclizumab effects in our study, including IL-6 cytokine regulatory properties and a substantial concomitant drop in INFc. Concurrently, Daclizumab treatment triggered a significant reduction in both the uveal histopathological grading and protein concentration in aqueous humors, but not in cellular infiltration. | ca_CA |
dc.format.extent | 8 p. | ca_CA |
dc.format.mimetype | application/pdf | ca_CA |
dc.language.iso | eng | ca_CA |
dc.publisher | Public Library of Science | ca_CA |
dc.relation.isPartOf | PLOS ONE, March 2014, Volume 9, Issue 3, e90216 | ca_CA |
dc.rights | © 2014 Mérida et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. | ca_CA |
dc.rights | Attribution 4.0 Spain | * |
dc.rights.uri | http://creativecommons.org/licenses/by-sa/4.0/ | * |
dc.title | An anti-interleukin-2 receptor drug attenuates thelper 1 lymphocytes-mediated inflammation in an acute model of endotoxin-induced uveitis | ca_CA |
dc.type | info:eu-repo/semantics/article | ca_CA |
dc.identifier.doi | http://dx.doi.org/10.1371/journal.pone.0090216 | |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | ca_CA |
dc.relation.publisherVersion | http://www.plosone.org/article/fetchObject.action?uri=info:doi/10.1371/journal.pone.0090216&representation=PDF | ca_CA |
dc.type.version | info:eu-repo/semantics/publishedVersion |
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Except where otherwise noted, this item's license is described as © 2014 Mérida et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.