EX-vivo whole blood stimulation with A2E does not elicit an inflammatory cytokine response in patients with age-related macular degeneration

Abstract Age-related macular degeneration (AMD) is a highly prevalent degenerative disease and a leading cause of vision loss worldwide. Evidence for an inflammatory component in the development of AMD exists, yet the exact mechanisms remain unclear. Bisretinoid N-retinylidene-N-retinylethanolamine...

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Autores principales: Jon Ambæk Durhuus, Maarten P. Rozing, Marie Krogh Nielsen, Christopher Rue Molbech, Guido Keijzers, Morten Scheibye-Knudsen, Lene Juel Rasmussen, Rudi G. J. Westendorp, Torben Lykke Sørensen
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Publicado: Nature Portfolio 2021
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spelling oai:doaj.org-article:90a31db0e9514fae98b0ee165a94d82a2021-12-02T14:30:46ZEX-vivo whole blood stimulation with A2E does not elicit an inflammatory cytokine response in patients with age-related macular degeneration10.1038/s41598-021-87337-12045-2322https://doaj.org/article/90a31db0e9514fae98b0ee165a94d82a2021-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-87337-1https://doaj.org/toc/2045-2322Abstract Age-related macular degeneration (AMD) is a highly prevalent degenerative disease and a leading cause of vision loss worldwide. Evidence for an inflammatory component in the development of AMD exists, yet the exact mechanisms remain unclear. Bisretinoid N-retinylidene-N-retinylethanolamine (A2E) in retinal pigmental epithelial (RPE) cells, and in extracellular deposits constitutes a hallmark of AMD, but its role in the pathology of AMD is elusive. Here, we tested the hypothesis that A2E is responsible for the heightened inflammatory activity in AMD. To this end, we measured ex vivo mRNA expression of the cytokines TNF-α, IL-6, and IL-10 in whole blood samples after stimulation with A2E in a clinical sample of 27 patients with neovascular AMD and 24 patients with geographic atrophy secondary to AMD. Patients’ spouses (n = 30) were included as non-affected controls. After stimulation with A2E, no statistical differences were found in the median expression level of TNF-α, IL-6, IL-10 between the control group, and the neovascular AMD and the geographic atrophy group. Our findings do not support evidence for the hypothesis, that A2E per se contributes to heightened inflammatory activity in AMD.Jon Ambæk DurhuusMaarten P. RozingMarie Krogh NielsenChristopher Rue MolbechGuido KeijzersMorten Scheibye-KnudsenLene Juel RasmussenRudi G. J. WestendorpTorben Lykke SørensenNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-8 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Jon Ambæk Durhuus
Maarten P. Rozing
Marie Krogh Nielsen
Christopher Rue Molbech
Guido Keijzers
Morten Scheibye-Knudsen
Lene Juel Rasmussen
Rudi G. J. Westendorp
Torben Lykke Sørensen
EX-vivo whole blood stimulation with A2E does not elicit an inflammatory cytokine response in patients with age-related macular degeneration
description Abstract Age-related macular degeneration (AMD) is a highly prevalent degenerative disease and a leading cause of vision loss worldwide. Evidence for an inflammatory component in the development of AMD exists, yet the exact mechanisms remain unclear. Bisretinoid N-retinylidene-N-retinylethanolamine (A2E) in retinal pigmental epithelial (RPE) cells, and in extracellular deposits constitutes a hallmark of AMD, but its role in the pathology of AMD is elusive. Here, we tested the hypothesis that A2E is responsible for the heightened inflammatory activity in AMD. To this end, we measured ex vivo mRNA expression of the cytokines TNF-α, IL-6, and IL-10 in whole blood samples after stimulation with A2E in a clinical sample of 27 patients with neovascular AMD and 24 patients with geographic atrophy secondary to AMD. Patients’ spouses (n = 30) were included as non-affected controls. After stimulation with A2E, no statistical differences were found in the median expression level of TNF-α, IL-6, IL-10 between the control group, and the neovascular AMD and the geographic atrophy group. Our findings do not support evidence for the hypothesis, that A2E per se contributes to heightened inflammatory activity in AMD.
format article
author Jon Ambæk Durhuus
Maarten P. Rozing
Marie Krogh Nielsen
Christopher Rue Molbech
Guido Keijzers
Morten Scheibye-Knudsen
Lene Juel Rasmussen
Rudi G. J. Westendorp
Torben Lykke Sørensen
author_facet Jon Ambæk Durhuus
Maarten P. Rozing
Marie Krogh Nielsen
Christopher Rue Molbech
Guido Keijzers
Morten Scheibye-Knudsen
Lene Juel Rasmussen
Rudi G. J. Westendorp
Torben Lykke Sørensen
author_sort Jon Ambæk Durhuus
title EX-vivo whole blood stimulation with A2E does not elicit an inflammatory cytokine response in patients with age-related macular degeneration
title_short EX-vivo whole blood stimulation with A2E does not elicit an inflammatory cytokine response in patients with age-related macular degeneration
title_full EX-vivo whole blood stimulation with A2E does not elicit an inflammatory cytokine response in patients with age-related macular degeneration
title_fullStr EX-vivo whole blood stimulation with A2E does not elicit an inflammatory cytokine response in patients with age-related macular degeneration
title_full_unstemmed EX-vivo whole blood stimulation with A2E does not elicit an inflammatory cytokine response in patients with age-related macular degeneration
title_sort ex-vivo whole blood stimulation with a2e does not elicit an inflammatory cytokine response in patients with age-related macular degeneration
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/90a31db0e9514fae98b0ee165a94d82a
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