In utero bacterial endotoxin exposure causes loss of tyrosine hydroxylase neurons in the postnatal rat midbrain.
Identifieur interne : 003B90 ( PubMed/Corpus ); précédent : 003B89; suivant : 003B91In utero bacterial endotoxin exposure causes loss of tyrosine hydroxylase neurons in the postnatal rat midbrain.
Auteurs : Zaodung Ling ; Dave A. Gayle ; Shang Yong Ma ; Jack W. Lipton ; Chong Wai Tong ; Jau-Shyong Hong ; Paul M. CarveySource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2002.
English descriptors
- KwdEn :
- Animals, Animals, Newborn, Corpus Striatum (immunology), Corpus Striatum (metabolism), Dopamine (metabolism), Endotoxins (metabolism), Female, Fetal Diseases (immunology), Fetal Diseases (metabolism), Gestational Age, Immunohistochemistry, Interleukin-1 (immunology), Mesencephalon (immunology), Mesencephalon (metabolism), Parkinson Disease (immunology), Parkinson Disease (metabolism), Pregnancy, Prenatal Exposure Delayed Effects, Rats, Rats, Sprague-Dawley, Risk Factors, Tumor Necrosis Factor-alpha (immunology), Tyrosine 3-Monooxygenase (deficiency).
- MESH :
- chemical , deficiency : Tyrosine 3-Monooxygenase.
- chemical , immunology : Interleukin-1, Tumor Necrosis Factor-alpha.
- chemical , metabolism : Dopamine, Endotoxins.
- immunology : Corpus Striatum, Fetal Diseases, Mesencephalon, Parkinson Disease.
- metabolism : Corpus Striatum, Fetal Diseases, Mesencephalon, Parkinson Disease.
- Animals, Animals, Newborn, Female, Gestational Age, Immunohistochemistry, Pregnancy, Prenatal Exposure Delayed Effects, Rats, Rats, Sprague-Dawley, Risk Factors.
Abstract
We investigated whether in utero exposure to the Gram(-) bacteriotoxin lipopolysaccharide (LPS) induces dopamine (DA) neuron loss in rats. The proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha) kills DA neurons and is elevated in the brains of patients with Parkinson's disease (PD). LPS is a potent inducer of TNF-alpha, and both are increased in the chorioamniotic environment of women who have bacterial vaginosis (BV) during pregnancy, suggesting that BV might interfere with the normal development of fetal DA neurons. Gravid female rats were injected intraperitoneally with either LPS or normal saline at embryonic day 10.5 and their pups were killed at postnatal day 21. The brains of the pups were assessed for DA and TNF-alpha levels and DA cell counts in the mesencephalon using tyrosine hydroxylase immunoreactive (THir) cells as a DA neuron marker. Prenatal LPS exposure significantly reduced striatal DA (29%) and increased DA activity (72%) as well as TNF-alpha (101%). Stereological cell counts in the mesencephalon were also significantly reduced (27%) by prenatal LPS exposure. Prenatal exposure to LPS, as might occur in humans with BV, produces a significant loss of THir cells in rats that is still present 33 days following a single injection of LPS. Since this cell loss is well past the normal phase of DA neuron apoptosis that occurs in early postnatal life, rats so exposed may have a permanent loss of DA neurons, suggesting that prenatal infections may represent risk factors for PD.
PubMed: 11835448
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pubmed:11835448Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">In utero bacterial endotoxin exposure causes loss of tyrosine hydroxylase neurons in the postnatal rat midbrain.</title><author><name sortKey="Ling, Zaodung" sort="Ling, Zaodung" uniqKey="Ling Z" first="Zaodung" last="Ling">Zaodung Ling</name><affiliation><nlm:affiliation>Department of Pharmacology, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois, USA. zling@rush.edu</nlm:affiliation></affiliation></author><author><name sortKey="Gayle, Dave A" sort="Gayle, Dave A" uniqKey="Gayle D" first="Dave A" last="Gayle">Dave A. Gayle</name></author><author><name sortKey="Ma, Shang Yong" sort="Ma, Shang Yong" uniqKey="Ma S" first="Shang Yong" last="Ma">Shang Yong Ma</name></author><author><name sortKey="Lipton, Jack W" sort="Lipton, Jack W" uniqKey="Lipton J" first="Jack W" last="Lipton">Jack W. Lipton</name></author><author><name sortKey="Tong, Chong Wai" sort="Tong, Chong Wai" uniqKey="Tong C" first="Chong Wai" last="Tong">Chong Wai Tong</name></author><author><name sortKey="Hong, Jau Shyong" sort="Hong, Jau Shyong" uniqKey="Hong J" first="Jau-Shyong" last="Hong">Jau-Shyong Hong</name></author><author><name sortKey="Carvey, Paul M" sort="Carvey, Paul M" uniqKey="Carvey P" first="Paul M" last="Carvey">Paul M. Carvey</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:11835448</idno><idno type="pmid">11835448</idno><idno type="wicri:Area/PubMed/Corpus">003B90</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">In utero bacterial endotoxin exposure causes loss of tyrosine hydroxylase neurons in the postnatal rat midbrain.</title><author><name sortKey="Ling, Zaodung" sort="Ling, Zaodung" uniqKey="Ling Z" first="Zaodung" last="Ling">Zaodung Ling</name><affiliation><nlm:affiliation>Department of Pharmacology, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois, USA. zling@rush.edu</nlm:affiliation></affiliation></author><author><name sortKey="Gayle, Dave A" sort="Gayle, Dave A" uniqKey="Gayle D" first="Dave A" last="Gayle">Dave A. Gayle</name></author><author><name sortKey="Ma, Shang Yong" sort="Ma, Shang Yong" uniqKey="Ma S" first="Shang Yong" last="Ma">Shang Yong Ma</name></author><author><name sortKey="Lipton, Jack W" sort="Lipton, Jack W" uniqKey="Lipton J" first="Jack W" last="Lipton">Jack W. Lipton</name></author><author><name sortKey="Tong, Chong Wai" sort="Tong, Chong Wai" uniqKey="Tong C" first="Chong Wai" last="Tong">Chong Wai Tong</name></author><author><name sortKey="Hong, Jau Shyong" sort="Hong, Jau Shyong" uniqKey="Hong J" first="Jau-Shyong" last="Hong">Jau-Shyong Hong</name></author><author><name sortKey="Carvey, Paul M" sort="Carvey, Paul M" uniqKey="Carvey P" first="Paul M" last="Carvey">Paul M. Carvey</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Animals, Newborn</term><term>Corpus Striatum (immunology)</term><term>Corpus Striatum (metabolism)</term><term>Dopamine (metabolism)</term><term>Endotoxins (metabolism)</term><term>Female</term><term>Fetal Diseases (immunology)</term><term>Fetal Diseases (metabolism)</term><term>Gestational Age</term><term>Immunohistochemistry</term><term>Interleukin-1 (immunology)</term><term>Mesencephalon (immunology)</term><term>Mesencephalon (metabolism)</term><term>Parkinson Disease (immunology)</term><term>Parkinson Disease (metabolism)</term><term>Pregnancy</term><term>Prenatal Exposure Delayed Effects</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Risk Factors</term><term>Tumor Necrosis Factor-alpha (immunology)</term><term>Tyrosine 3-Monooxygenase (deficiency)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Interleukin-1</term><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>Endotoxins</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Corpus Striatum</term><term>Fetal Diseases</term><term>Mesencephalon</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>Fetal Diseases</term><term>Mesencephalon</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Animals, Newborn</term><term>Female</term><term>Gestational Age</term><term>Immunohistochemistry</term><term>Pregnancy</term><term>Prenatal Exposure Delayed Effects</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Risk Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We investigated whether in utero exposure to the Gram(-) bacteriotoxin lipopolysaccharide (LPS) induces dopamine (DA) neuron loss in rats. The proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha) kills DA neurons and is elevated in the brains of patients with Parkinson's disease (PD). LPS is a potent inducer of TNF-alpha, and both are increased in the chorioamniotic environment of women who have bacterial vaginosis (BV) during pregnancy, suggesting that BV might interfere with the normal development of fetal DA neurons. Gravid female rats were injected intraperitoneally with either LPS or normal saline at embryonic day 10.5 and their pups were killed at postnatal day 21. The brains of the pups were assessed for DA and TNF-alpha levels and DA cell counts in the mesencephalon using tyrosine hydroxylase immunoreactive (THir) cells as a DA neuron marker. Prenatal LPS exposure significantly reduced striatal DA (29%) and increased DA activity (72%) as well as TNF-alpha (101%). Stereological cell counts in the mesencephalon were also significantly reduced (27%) by prenatal LPS exposure. Prenatal exposure to LPS, as might occur in humans with BV, produces a significant loss of THir cells in rats that is still present 33 days following a single injection of LPS. Since this cell loss is well past the normal phase of DA neuron apoptosis that occurs in early postnatal life, rats so exposed may have a permanent loss of DA neurons, suggesting that prenatal infections may represent risk factors for PD.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">11835448</PMID><DateCreated><Year>2002</Year><Month>02</Month><Day>08</Day></DateCreated><DateCompleted><Year>2002</Year><Month>05</Month><Day>24</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>17</Volume><Issue>1</Issue><PubDate><Year>2002</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>In utero bacterial endotoxin exposure causes loss of tyrosine hydroxylase neurons in the postnatal rat midbrain.</ArticleTitle><Pagination><MedlinePgn>116-24</MedlinePgn></Pagination><Abstract><AbstractText>We investigated whether in utero exposure to the Gram(-) bacteriotoxin lipopolysaccharide (LPS) induces dopamine (DA) neuron loss in rats. The proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha) kills DA neurons and is elevated in the brains of patients with Parkinson's disease (PD). LPS is a potent inducer of TNF-alpha, and both are increased in the chorioamniotic environment of women who have bacterial vaginosis (BV) during pregnancy, suggesting that BV might interfere with the normal development of fetal DA neurons. Gravid female rats were injected intraperitoneally with either LPS or normal saline at embryonic day 10.5 and their pups were killed at postnatal day 21. The brains of the pups were assessed for DA and TNF-alpha levels and DA cell counts in the mesencephalon using tyrosine hydroxylase immunoreactive (THir) cells as a DA neuron marker. Prenatal LPS exposure significantly reduced striatal DA (29%) and increased DA activity (72%) as well as TNF-alpha (101%). Stereological cell counts in the mesencephalon were also significantly reduced (27%) by prenatal LPS exposure. Prenatal exposure to LPS, as might occur in humans with BV, produces a significant loss of THir cells in rats that is still present 33 days following a single injection of LPS. Since this cell loss is well past the normal phase of DA neuron apoptosis that occurs in early postnatal life, rats so exposed may have a permanent loss of DA neurons, suggesting that prenatal infections may represent risk factors for PD.</AbstractText><CopyrightInformation>Copyright 2001 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ling</LastName><ForeName>ZaoDung</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Pharmacology, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois, USA. zling@rush.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gayle</LastName><ForeName>Dave A</ForeName><Initials>DA</Initials></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Shang Yong</ForeName><Initials>SY</Initials></Author><Author ValidYN="Y"><LastName>Lipton</LastName><ForeName>Jack W</ForeName><Initials>JW</Initials></Author><Author ValidYN="Y"><LastName>Tong</LastName><ForeName>Chong Wai</ForeName><Initials>CW</Initials></Author><Author ValidYN="Y"><LastName>Hong</LastName><ForeName>Jau-Shyong</ForeName><Initials>JS</Initials></Author><Author ValidYN="Y"><LastName>Carvey</LastName><ForeName>Paul M</ForeName><Initials>PM</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>ES10776</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004731">Endotoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007375">Interleukin-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.16.2</RegistryNumber><NameOfSubstance UI="D014446">Tyrosine 3-Monooxygenase</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000831">Animals, Newborn</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003342">Corpus Striatum</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000276">immunology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004298">Dopamine</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004731">Endotoxins</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005315">Fetal Diseases</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000276">immunology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005865">Gestational Age</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007150">Immunohistochemistry</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007375">Interleukin-1</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000276">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008636">Mesencephalon</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000276">immunology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000276">immunology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011247">Pregnancy</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D011297">Prenatal Exposure Delayed Effects</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051381">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017207">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012307">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014409">Tumor Necrosis Factor-alpha</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000276">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014446">Tyrosine 3-Monooxygenase</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000172">deficiency</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2002</Year><Month>2</Month><Day>9</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2002</Year><Month>5</Month><Day>25</Day><Hour>10</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2002</Year><Month>2</Month><Day>9</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">11835448</ArticleId><ArticleId IdType="pii">10.1002/mds.10078</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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