Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/42909
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dc.contributor.authorMingo, Yakum Benard-
dc.contributor.authorGabele, Lea-
dc.contributor.authorLonnemann, Niklas-
dc.contributor.authorBRONE, Bert-
dc.contributor.authorKorte, Martin-
dc.contributor.authorHosseini, Shirin-
dc.date.accessioned2024-05-13T11:17:29Z-
dc.date.available2024-05-13T11:17:29Z-
dc.date.issued2024-
dc.date.submitted2024-05-13T08:31:21Z-
dc.identifier.citationFrontiers in Cellular Neuroscience, 18 (Art N° 1343562)-
dc.identifier.issn-
dc.identifier.urihttp://hdl.handle.net/1942/42909-
dc.description.abstractNeuroinflammation can be triggered by various stimuli, including viral infections. Viruses can directly invade the brain and infect neuronal cells or indirectly trigger a "cytokine storm" in the periphery that eventually leads to microglial activation in the brain. While this initial activation of microglial cells is important for viral clearance, chronic activation leads to excessive inflammation and oxidative stress, which can be neurotoxic. Remarkebly, recent studies have shown that certain viruses such as influenza A virus, coronavirus, herpes virus and Epstein-Barr virus may be involved in the development of neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, and multiple sclerosis. Therefore, it is important to find therapeutic strategies against chronic neuroinflammation triggered by viral infections. Here, we investigated the effects of urolithin A (UA) on microglial activation in vitro induced by a viral mimetic, poly I:C, in a triple co-culture system of neurons, astrocytes and microglial cells. Immunocytochemistry was used to perform a comprehensive single-cell analysis of the morphological changes of microglia as an indicator of their reactive state. Treatment with UA significantly prevented the poly I:C-induced reactive state of microglia, which was characterized by increased expression of the microglial activation markers CD68 and IBA-1. UA restored the poly I:C-induced morphology by restoring microglial ramification. In addition, UA was able to reduce the release of the pro-inflammatory mediators CCL2, TNF-alpha, and IL-1 beta and showed a trend toward attenuation of cellular ROS production in poly I:C-treated cultures. Overall, this study suggests that UA as a component of a healthy diet may help prevent virus-induced neuroinflammation and may have therapeutic potential for future studies to prevent or treat neurodegenerative diseases by targeting the associated neuroinflammatory processes.-
dc.description.sponsorshipThe authors would like to thank the members of the Department of Cellular Neurobiology at the Zoological Institute of the TU Braunschweig. We also thank a lot Tania Meßerschmidt, Diane Mundil, and Tina Geisler for their excellent technical support.-
dc.language.isoen-
dc.publisherFRONTIERS MEDIA SA-
dc.rights2024 Mingo, Gabele, Lonnemann, Brône, Korte and Hosseini. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.-
dc.subject.otherpoly I:C-
dc.subject.othermicroglial activation-
dc.subject.otherneuroinflammation-
dc.subject.otheroxidative stress-
dc.subject.otherurolithin A-
dc.titleThe effects of urolithin A on poly I:C-induced microglial activation-
dc.typeJournal Contribution-
dc.identifier.volume18-
local.format.pages15-
local.bibliographicCitation.jcatA1-
dc.description.notesHosseini, S (corresponding author), Tech Univ Carolo Wilhelmina Braunschweig, Zool Inst, Dept Cellular Neurobiol, Braunschweig, Germany.; Hosseini, S (corresponding author), Helmholtz Ctr Infect Res, Res Grp Neuroinflammat & Neurodegenerat, Braunschweig, Germany.-
dc.description.notess.hosseini@tu-braunschweig.de-
local.publisher.placeAVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND-
local.type.refereedRefereed-
local.type.specifiedArticle-
local.bibliographicCitation.artnr1343562-
dc.identifier.doi10.3389/fncel.2024.1343562-
dc.identifier.pmid38577490-
dc.identifier.isi001195815700001-
dc.contributor.orcidBenard Mingo, Yakum/0000-0002-8208-8522-
local.provider.typewosris-
local.description.affiliation[Mingo, Yakum Benard; Gabele, Lea; Lonnemann, Niklas; Korte, Martin; Hosseini, Shirin] Tech Univ Carolo Wilhelmina Braunschweig, Zool Inst, Dept Cellular Neurobiol, Braunschweig, Germany.-
local.description.affiliation[Mingo, Yakum Benard; Brone, Bert] Hasselt Univ, Biomed Res Inst, Lab Neurophysiol, Hasselt, Belgium.-
local.description.affiliation[Gabele, Lea; Korte, Martin; Hosseini, Shirin] Helmholtz Ctr Infect Res, Res Grp Neuroinflammat & Neurodegenerat, Braunschweig, Germany.-
local.uhasselt.internationalyes-
item.fullcitationMingo, Yakum Benard; Gabele, Lea; Lonnemann, Niklas; BRONE, Bert; Korte, Martin & Hosseini, Shirin (2024) The effects of urolithin A on poly I:C-induced microglial activation. In: Frontiers in Cellular Neuroscience, 18 (Art N° 1343562).-
item.fulltextWith Fulltext-
item.contributorMingo, Yakum Benard-
item.contributorGabele, Lea-
item.contributorLonnemann, Niklas-
item.contributorBRONE, Bert-
item.contributorKorte, Martin-
item.contributorHosseini, Shirin-
item.accessRightsOpen Access-
crisitem.journal.eissn1662-5102-
Appears in Collections:Research publications
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