Acute in utero exposure to lipopolysaccharide induces inflammation in the pre- and postnatal brain and alters the glial cytoarchitecture in the developing amygdala

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dc.contributor.author O'Loughlin, Elaine
dc.contributor.author Pakan, Janelle M. P.
dc.contributor.author Yilmazer-Hanke, Deniz
dc.contributor.author McDermott, Kieran W.
dc.date.accessioned 2018-06-15T11:47:08Z
dc.date.available 2018-06-15T11:47:08Z
dc.date.issued 2017
dc.identifier.citation O’Loughlin, E., Pakan, J. M. P., Yilmazer-Hanke, D. and McDermott, K. W. (2017) 'Acute in utero exposure to lipopolysaccharide induces inflammation in the pre- and postnatal brain and alters the glial cytoarchitecture in the developing amygdala', Journal of Neuroinflammation, 14, 212 (12pp). doi: 10.1186/s12974-017-0981-8 en
dc.identifier.volume 14
dc.identifier.startpage 1
dc.identifier.endpage 12
dc.identifier.issn 1742-2094
dc.identifier.uri http://hdl.handle.net/10468/6318
dc.identifier.doi 10.1186/s12974-017-0981-8
dc.description.abstract Background: Maternal immune activation (MIA) is a risk factor for neurodevelopmental disorders such as autism and schizophrenia, as well as seizure development. The amygdala is a brain region involved in the regulation of emotions, and amygdalar maldevelopment due to infection-induced MIA may lead to amygdala-related disorders. MIA priming of glial cells during development has been linked to abnormalities seen in later life; however, little is known about its effects on amygdalar biochemical and cytoarchitecture integrity. Methods: Time-mated C57BL6J mice were administered a single intraperitoneal injection of 50 mu g/kg lipopolysaccharide (LPS) on embryonic day 12 (E12), and the effects of MIA were examined at prenatal, neonatal, and postnatal developmental stages using immunohistochemistry, real-time quantitative PCR, and stereological quantification of cytoarchitecture changes. Results: Fetal brain expression of pro-inflammatory cytokines (IL-1 beta, TNF alpha, and IL-6) was significantly upregulated at 4 h postinjection (E12) and remained elevated until the day of birth (P0). In offspring from LPS-treated dams, amygdalar expression of pro-inflammatory cytokines was also increased on day 7 (P7) and expression was sustained on day 40 (P40). Toll-like receptor (TLR-2, TLR-4) expression was also upregulated in fetal brains and in the postnatal amygdala in LPS-injected animals. Morphological examination of cells expressing ionized calcium-binding adaptor molecule 1 (Iba-1) and glial fibrillary acidic protein (GFAP) suggested long-term microglial activation and astrogliosis in postnatal amygdalar regions. Conclusions: Our results showed that LPS-induced MIA at E12 induces a pro-inflammatory cytokine profile in the developing fetal brain that continues up to early adulthood in the amygdala. Inflammation elicited by MIA may activate cells in the fetal brain and lead to alterations in glial (microglia and astrocyte) cells observed in the postnatal amygdala. Moreover, increased pro-inflammatory cytokines and their effects on glial subpopulations may in turn have deleterious consequences for neuronal viability. These MIA-induced changes may predispose offspring to amygdala-related disorders such as heightened anxiety and depression and also neurodevelopmental disorders, such as autism spectrum disorders. en
dc.description.sponsorship Health Research Board (HRA_POR/2010/159) en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher BioMed Central Ltd. en
dc.relation.uri https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-017-0981-8
dc.rights © 2017, the Authors. Open Access. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. en
dc.rights.uri http://creativecommons.org/licenses/by/4.0/
dc.subject Maternal inflammation en
dc.subject Amygdala en
dc.subject Neuroinflammation en
dc.subject Neurodevelopment en
dc.subject Amygdalar development en
dc.subject Inflammatory cytokines en
dc.subject Microglia en
dc.subject Astrogliosis en
dc.subject Lipopolysaccharide en
dc.title Acute in utero exposure to lipopolysaccharide induces inflammation in the pre- and postnatal brain and alters the glial cytoarchitecture in the developing amygdala en
dc.type Article (peer-reviewed) en
dc.internal.authorcontactother Kieran McDermott, Anatomy and Neuroscience, University College Cork, Cork, Ireland. +353-21-490-3000 Email: kmcd@ucc.ie en
dc.internal.availability Full text available en
dc.description.version Published Version en
dc.contributor.funder Health Research Board
dc.description.status Peer reviewed
dc.identifier.journaltitle Journal of Neuroinflammation en
dc.internal.IRISemailaddress kmcd@ucc.ie en
dc.identifier.articleid 212


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© 2017, the Authors. Open Access. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Except where otherwise noted, this item's license is described as © 2017, the Authors. Open Access. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
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