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IL-10 and Cdc42 as critical modulators in methamphtamine-induced neuroinflammation

2024-04-05Póster em conferência Acesso aberto
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dc.contributor.authorSilva, Ana Isabel
dc.contributor.authorSocodato, Renato
dc.contributor.authorPinto, Carolina
dc.contributor.authorTerceiro, Ana Filipa
dc.contributor.authorCanedo, Teresa
dc.contributor.authorRelvas, João Bettencourt
dc.contributor.authorSaraiva, Margarida
dc.contributor.authorSummavielle, Teresa
dc.contributor.authorSummavielle, Teresa
dc.date.accessioned2026-01-22T09:17:45Z
dc.date.available2026-01-22T09:17:45Z
dc.date.issued2024-04-05
dc.description.abstractPsychoactive substances, such as Methamphetamine (Meth), can induce complex neuroinflammatory responses that modulate the neuron-glia cross talk and strongly affect behavioral responses. Recently we have reported that Meth stimulates astrocytes to release tumor necrosis factor (TNF) and glutamate, leading to microglial activation, microgliosis and loss of risk-assessment. Here, we started by investigating the anti-inflammatory power the cytokine interleukin-10 (IL-10), resorting to astrocyte and microglia primary transfected with different FRET probes and exposed to Meth (100µM), to elucidate the mechanisms involved. Then after, we confirmed these results in vivo, by employing a transgenic mouse model that overexpresses IL-10 (pMT-10), in time-controlled manner, and administering a binge Meth dosing (4 x 5mg/kg, with 2h intervals). In vitro, our findings reveal that the presence of recombinant IL-10 (rIL-10) counteracts Meth-induced excessive glutamate release in astrocytes, which significantly reduced microglial activation. This reduction was associated with the modulation of astrocytic intracellular calcium (Ca2+) dynamics, particularly by restricting the release of Ca2+ from the endoplasmic reticulum to the cytoplasm. Furthermore, we identify the small Rho GTPase Cdc42 as a crucial intermediary in the astrocyte-to-microglia communication pathway under Meth. In vivo, we observed that IL-10 overexpressing prevented Meth-induced neuroinflammation, microgliosis and Meth-induced behavioral changes. These findings enhance our understanding of Meth-related neuroinflammatory mechanisms, suggesting IL-10 and Cdc42 as putative therapeutic targets, and strengthen the view of a neuroimmune nature for addiction.eng
dc.identifier.citationSilva, A. I., Socodato, R., Pinto, C., Terceiro, A. F., Canedo, T., Relvas, J. B., Saraiva, M., & Summavielle, T. (2024). IL-10 and Cdc42 as critical modulators in methamphtamine-induced neuroinflammation. VII Symposium Portuguese Glial Network - Abstract Book, 37–38. https://redeglial.weebly.com/uploads/8/9/4/3/89438276/abstract_book_1.pdf
dc.identifier.urihttp://hdl.handle.net/10400.22/31598
dc.language.isoeng
dc.peerreviewedyes
dc.publisherICVS - School of Medicine
dc.relationPTDC/SAU-TOX/0067/2021; SFRH/BD/144324/2019, 2020.07188.BD; 2022.03699.CEECIND and CEECIND/00241/2017
dc.relation.hasversionhttps://redeglial.weebly.com/uploads/8/9/4/3/89438276/abstract_book_1.pdf
dc.rights.uriN/A
dc.subjectMethamphetamine (Meth)
dc.subjecttumor necrosis factor (TNF)
dc.subjectinterleukin-10 (IL-10)
dc.titleIL-10 and Cdc42 as critical modulators in methamphtamine-induced neuroinflammationeng
dc.typeconference poster
dspace.entity.typePublication
oaire.citation.conferenceDate2024-04-05
oaire.citation.conferencePlaceBraga
oaire.citation.endPage38
oaire.citation.startPage37
oaire.citation.titleVII Symposium Portuguese Glial Network - Abstract Book
oaire.versionhttp://purl.org/coar/version/c_970fb48d4fbd8a85
person.familyNameSummavielle
person.givenNameTeresa
person.identifier677706
person.identifier.ciencia-idC41E-0816-5C85
person.identifier.orcid0000-0003-2548-6281
person.identifier.ridC-9776-2012
person.identifier.scopus-author-id6603092949
relation.isAuthorOfPublication207ee2de-85a0-4144-9e7e-b376c600e065
relation.isAuthorOfPublication.latestForDiscovery207ee2de-85a0-4144-9e7e-b376c600e065

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