Maternal immune activation induces sustained changes in fetal microglia motility

Abstract Maternal infection or inflammation causes abnormalities in brain development associated with subsequent cognitive impairment and in an increased susceptibility to schizophrenia and autism spectrum disorders. Maternal immune activation (MIA) and increases in serum cytokine levels mediates th...

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Autores principales: Kana Ozaki, Daisuke Kato, Ako Ikegami, Akari Hashimoto, Shouta Sugio, Zhongtian Guo, Midori Shibushita, Tsuyako Tatematsu, Koichiro Haruwaka, Andrew J. Moorhouse, Hideto Yamada, Hiroaki Wake
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Publicado: Nature Portfolio 2020
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Acceso en línea:https://doaj.org/article/979f3c83c7a34bd2aeab127d90ed220a
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spelling oai:doaj.org-article:979f3c83c7a34bd2aeab127d90ed220a2021-12-02T12:33:45ZMaternal immune activation induces sustained changes in fetal microglia motility10.1038/s41598-020-78294-22045-2322https://doaj.org/article/979f3c83c7a34bd2aeab127d90ed220a2020-12-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-78294-2https://doaj.org/toc/2045-2322Abstract Maternal infection or inflammation causes abnormalities in brain development associated with subsequent cognitive impairment and in an increased susceptibility to schizophrenia and autism spectrum disorders. Maternal immune activation (MIA) and increases in serum cytokine levels mediates this association via effects on the fetal brain, and microglia can respond to maternal immune status, but consensus on how microglia may respond is lacking and no-one has yet examined if microglial process motility is impaired. In this study we investigated how MIA induced at two different gestational ages affected microglial properties at different developmental stages. Immune activation in mid-pregnancy increased IL-6 expression in embryonic microglia, but failed to cause any marked changes in morphology either at E18 or postnatally. In contrast MIA, particularly when induced earlier (at E12), caused sustained alterations in the patterns of microglial process motility and behavioral deficits. Our research has identified an important microglial property that is altered by MIA and which may contribute to the underlying pathophysiological mechanisms linking maternal immune status to subsequent risks for cognitive disease.Kana OzakiDaisuke KatoAko IkegamiAkari HashimotoShouta SugioZhongtian GuoMidori ShibushitaTsuyako TatematsuKoichiro HaruwakaAndrew J. MoorhouseHideto YamadaHiroaki WakeNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 10, Iss 1, Pp 1-19 (2020)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Kana Ozaki
Daisuke Kato
Ako Ikegami
Akari Hashimoto
Shouta Sugio
Zhongtian Guo
Midori Shibushita
Tsuyako Tatematsu
Koichiro Haruwaka
Andrew J. Moorhouse
Hideto Yamada
Hiroaki Wake
Maternal immune activation induces sustained changes in fetal microglia motility
description Abstract Maternal infection or inflammation causes abnormalities in brain development associated with subsequent cognitive impairment and in an increased susceptibility to schizophrenia and autism spectrum disorders. Maternal immune activation (MIA) and increases in serum cytokine levels mediates this association via effects on the fetal brain, and microglia can respond to maternal immune status, but consensus on how microglia may respond is lacking and no-one has yet examined if microglial process motility is impaired. In this study we investigated how MIA induced at two different gestational ages affected microglial properties at different developmental stages. Immune activation in mid-pregnancy increased IL-6 expression in embryonic microglia, but failed to cause any marked changes in morphology either at E18 or postnatally. In contrast MIA, particularly when induced earlier (at E12), caused sustained alterations in the patterns of microglial process motility and behavioral deficits. Our research has identified an important microglial property that is altered by MIA and which may contribute to the underlying pathophysiological mechanisms linking maternal immune status to subsequent risks for cognitive disease.
format article
author Kana Ozaki
Daisuke Kato
Ako Ikegami
Akari Hashimoto
Shouta Sugio
Zhongtian Guo
Midori Shibushita
Tsuyako Tatematsu
Koichiro Haruwaka
Andrew J. Moorhouse
Hideto Yamada
Hiroaki Wake
author_facet Kana Ozaki
Daisuke Kato
Ako Ikegami
Akari Hashimoto
Shouta Sugio
Zhongtian Guo
Midori Shibushita
Tsuyako Tatematsu
Koichiro Haruwaka
Andrew J. Moorhouse
Hideto Yamada
Hiroaki Wake
author_sort Kana Ozaki
title Maternal immune activation induces sustained changes in fetal microglia motility
title_short Maternal immune activation induces sustained changes in fetal microglia motility
title_full Maternal immune activation induces sustained changes in fetal microglia motility
title_fullStr Maternal immune activation induces sustained changes in fetal microglia motility
title_full_unstemmed Maternal immune activation induces sustained changes in fetal microglia motility
title_sort maternal immune activation induces sustained changes in fetal microglia motility
publisher Nature Portfolio
publishDate 2020
url https://doaj.org/article/979f3c83c7a34bd2aeab127d90ed220a
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