Expression of Alzheimer-Type Neurofibrillary Epitopes in Primary Rat Cortical Neurons Following Infection with Enterococcus faecalis
Identifieur interne : 000633 ( Pmc/Curation ); précédent : 000632; suivant : 000634Expression of Alzheimer-Type Neurofibrillary Epitopes in Primary Rat Cortical Neurons Following Infection with Enterococcus faecalis
Auteurs : Robert Underly [États-Unis] ; Mee-Sook Song [États-Unis] ; Gary L. Dunbar [États-Unis] ; Charles L. Weaver [États-Unis]Source :
- Frontiers in Aging Neuroscience [ 1663-4365 ] ; 2016.
Abstract
The neurofibrillary tau pathology and amyloid deposits seen in Alzheimer’s disease (AD) also have been seen in bacteria-infected brains. However, few studies have examined the role of these bacteria in the generation of tau pathology. One suggested link between infection and AD is edentulism, the complete loss of teeth. Edentulism can result from chronic periodontal disease due to infection by Infection increases Alz-50, phospho-Serine 202 tau, and MAP2 expression. Infection by
Url:
DOI: 10.3389/fnagi.2015.00259
PubMed: 26834627
PubMed Central: 4720002
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PMC:4720002Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Expression of Alzheimer-Type Neurofibrillary Epitopes in Primary Rat Cortical Neurons Following Infection with <italic>Enterococcus faecalis</italic>
</title>
<author><name sortKey="Underly, Robert" sort="Underly, Robert" uniqKey="Underly R" first="Robert" last="Underly">Robert Underly</name>
<affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Department of Psychology, Saginaw Valley State University</institution>
<country>University Center, MI, USA</country>
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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Song, Mee Sook" sort="Song, Mee Sook" uniqKey="Song M" first="Mee-Sook" last="Song">Mee-Sook Song</name>
<affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Field Neurosciences Institute</institution>
<country>Saginaw, MI, USA</country>
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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Dunbar, Gary L" sort="Dunbar, Gary L" uniqKey="Dunbar G" first="Gary L." last="Dunbar">Gary L. Dunbar</name>
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<country>Saginaw, MI, USA</country>
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<country xml:lang="fr">États-Unis</country>
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<affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Department of Psychology, Central Michigan University</institution>
<country>Mount Pleasant, MI, USA</country>
</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea></wicri:regionArea>
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<author><name sortKey="Weaver, Charles L" sort="Weaver, Charles L" uniqKey="Weaver C" first="Charles L." last="Weaver">Charles L. Weaver</name>
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<country>University Center, MI, USA</country>
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<series><title level="j">Frontiers in Aging Neuroscience</title>
<idno type="eISSN">1663-4365</idno>
<imprint><date when="2016">2016</date>
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<front><div type="abstract" xml:lang="en"><p>The neurofibrillary tau pathology and amyloid deposits seen in Alzheimer’s disease (AD) also have been seen in bacteria-infected brains. However, few studies have examined the role of these bacteria in the generation of tau pathology. One suggested link between infection and AD is edentulism, the complete loss of teeth. Edentulism can result from chronic periodontal disease due to infection by <italic>Enterococcus faecalis</italic>
. The current study assessed the ability to generate early Alzheimer-like neurofibrillary epitopes in primary rat cortical neurons through bacterial infection by <italic>E. faecalis</italic>
. Seven-day old cultured neurons were infected with <italic>E. faecalis</italic>
for 24 and 48 h. An upward molecular weight shift in tau by Western blotting (WB) and increased appearance of tau reactivity in cell bodies and degenerating neurites was found in the 48 h infection group for the antibody CP13 (phospho-Serine 202). A substantial increase in reactivity of Alz-50 was seen at 24 and 48 h after infection. Furthermore, extensive microtubule-associated protein 2 (MAP2) reactivity also was seen at 24 and 48 h post-infection. Our preliminary findings suggest a potential link between <italic>E. faecalis</italic>
infection and intracellular changes that may help facilitate early AD-like neurofibrillary pathology.
<list list-type="bullet"><title>Highlights</title>
<list-item><p><italic>Enterococcus faecalis</italic>
used in the generation of AD neurofibrillary epitopes in rat.</p>
</list-item>
<list-item><p>Infection increases Alz-50, phospho-Serine 202 tau, and MAP2 expression.</p>
</list-item>
<list-item><p>Infection by <italic>Enterococcus</italic>
may play a role in early Alzheimer neurofibrillary changes.</p>
</list-item>
</list>
</p>
</div>
</front>
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</TEI>
<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Front Aging Neurosci</journal-id>
<journal-id journal-id-type="iso-abbrev">Front Aging Neurosci</journal-id>
<journal-id journal-id-type="publisher-id">Front. Aging Neurosci.</journal-id>
<journal-title-group><journal-title>Frontiers in Aging Neuroscience</journal-title>
</journal-title-group>
<issn pub-type="epub">1663-4365</issn>
<publisher><publisher-name>Frontiers Media S.A.</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">26834627</article-id>
<article-id pub-id-type="pmc">4720002</article-id>
<article-id pub-id-type="doi">10.3389/fnagi.2015.00259</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Neuroscience</subject>
<subj-group><subject>Original Research</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group><article-title>Expression of Alzheimer-Type Neurofibrillary Epitopes in Primary Rat Cortical Neurons Following Infection with <italic>Enterococcus faecalis</italic>
</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Underly</surname>
<given-names>Robert</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/139478/overview"></uri>
</contrib>
<contrib contrib-type="author"><name><surname>Song</surname>
<given-names>Mee-Sook</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
<uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/264185/overview"></uri>
</contrib>
<contrib contrib-type="author"><name><surname>Dunbar</surname>
<given-names>Gary L.</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
<uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/264539/overview"></uri>
</contrib>
<contrib contrib-type="author"><name><surname>Weaver</surname>
<given-names>Charles L.</given-names>
</name>
<xref ref-type="aff" rid="aff4"><sup>4</sup>
</xref>
<xref ref-type="author-notes" rid="fn001"><sup>*</sup>
</xref>
<uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/263872/overview"></uri>
</contrib>
</contrib-group>
<aff id="aff1"><sup>1</sup>
<institution>Department of Psychology, Saginaw Valley State University</institution>
<country>University Center, MI, USA</country>
</aff>
<aff id="aff2"><sup>2</sup>
<institution>Field Neurosciences Institute</institution>
<country>Saginaw, MI, USA</country>
</aff>
<aff id="aff3"><sup>3</sup>
<institution>Department of Psychology, Central Michigan University</institution>
<country>Mount Pleasant, MI, USA</country>
</aff>
<aff id="aff4"><sup>4</sup>
<institution>Department of Health Sciences, Saginaw Valley State University</institution>
<country>University Center, MI, USA</country>
</aff>
<author-notes><fn fn-type="edited-by"><p>Edited by: Fernanda Laezza, University of Texas Medical Branch, USA</p>
</fn>
<fn fn-type="edited-by"><p>Reviewed by: Ramesh Kandimalla, Emory University, USA; Judith Miklossy, Prevention Alzheimer International Foundation and International Alzheimer Research Center, Switzerland</p>
</fn>
<corresp id="fn001">*Correspondence: Charles L. Weaver <email xlink:type="simple">clweave1@svsu.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="epub"><day>20</day>
<month>1</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="collection"><year>2015</year>
</pub-date>
<volume>7</volume>
<elocation-id>259</elocation-id>
<history><date date-type="received"><day>11</day>
<month>9</month>
<year>2015</year>
</date>
<date date-type="accepted"><day>24</day>
<month>12</month>
<year>2015</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2016 Underly, Song, Dunbar and Weaver.</copyright-statement>
<copyright-year>2016</copyright-year>
<copyright-holder>Underly, Song, Dunbar and Weaver</copyright-holder>
<license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor 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.</license-p>
</license>
</permissions>
<abstract><p>The neurofibrillary tau pathology and amyloid deposits seen in Alzheimer’s disease (AD) also have been seen in bacteria-infected brains. However, few studies have examined the role of these bacteria in the generation of tau pathology. One suggested link between infection and AD is edentulism, the complete loss of teeth. Edentulism can result from chronic periodontal disease due to infection by <italic>Enterococcus faecalis</italic>
. The current study assessed the ability to generate early Alzheimer-like neurofibrillary epitopes in primary rat cortical neurons through bacterial infection by <italic>E. faecalis</italic>
. Seven-day old cultured neurons were infected with <italic>E. faecalis</italic>
for 24 and 48 h. An upward molecular weight shift in tau by Western blotting (WB) and increased appearance of tau reactivity in cell bodies and degenerating neurites was found in the 48 h infection group for the antibody CP13 (phospho-Serine 202). A substantial increase in reactivity of Alz-50 was seen at 24 and 48 h after infection. Furthermore, extensive microtubule-associated protein 2 (MAP2) reactivity also was seen at 24 and 48 h post-infection. Our preliminary findings suggest a potential link between <italic>E. faecalis</italic>
infection and intracellular changes that may help facilitate early AD-like neurofibrillary pathology.
<list list-type="bullet"><title>Highlights</title>
<list-item><p><italic>Enterococcus faecalis</italic>
used in the generation of AD neurofibrillary epitopes in rat.</p>
</list-item>
<list-item><p>Infection increases Alz-50, phospho-Serine 202 tau, and MAP2 expression.</p>
</list-item>
<list-item><p>Infection by <italic>Enterococcus</italic>
may play a role in early Alzheimer neurofibrillary changes.</p>
</list-item>
</list>
</p>
</abstract>
<kwd-group><kwd>Alzheimer’s disease</kwd>
<kwd><italic>Enterococcus faecalis</italic>
</kwd>
<kwd>edentulism</kwd>
<kwd>chronic periodontitis</kwd>
<kwd>tau</kwd>
<kwd>phosphorylation</kwd>
<kwd>Alz-50</kwd>
</kwd-group>
<funding-group><award-group><funding-source id="cn001">Saginaw Valley State University Faculty Research Award</funding-source>
</award-group>
<award-group><funding-source id="cn002">Field Neurosciences Institution Collaboration Award</funding-source>
</award-group>
<award-group><funding-source id="cn003">Support of Mentors and Students - Underrepresented Minorities Award (SOMAS-URM)</funding-source>
</award-group>
</funding-group>
<counts><fig-count count="4"></fig-count>
<table-count count="0"></table-count>
<equation-count count="0"></equation-count>
<ref-count count="63"></ref-count>
<page-count count="8"></page-count>
<word-count count="5951"></word-count>
</counts>
</article-meta>
</front>
</pmc>
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