Phagocytic cell function in aged subjects.
Identifieur interne : 001867 ( PubMed/Corpus ); précédent : 001866; suivant : 001868Phagocytic cell function in aged subjects.
Auteurs : J L Mege ; C. Capo ; B. Michel ; J L Gastaut ; P. BongrandSource :
- Neurobiology of aging [ 0197-4580 ]
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Aging (metabolism), Alzheimer Disease (metabolism), Cytochrome c Group (metabolism), Erythrocytes (metabolism), Female, Granulocytes (metabolism), Humans, Male, Middle Aged, Monocytes (metabolism), Oxidation-Reduction, Parkinson Disease (metabolism), Phagocytosis, Zymosan.
- MESH :
- chemical , metabolism : Cytochrome c Group.
- metabolism : Aging, Alzheimer Disease, Erythrocytes, Granulocytes, Monocytes, Parkinson Disease.
- Adult, Aged, Aged, 80 and over, Female, Humans, Male, Middle Aged, Oxidation-Reduction, Phagocytosis, Zymosan.
Abstract
In order to study the activity of phagocytic cells in normal and pathological aging, we compared normal young and aged subjects and patients with Alzheimer's (AD) or Parkinson's (PD) disease. Blood granulocytes and monocytes were separately assayed for ingestion of three different particle species (opsonized zymosan, immunoglobulin-coated sheep red cells (IgG-SRC) and glutaraldehyde-treated sheep red cells (G-SRC]. The superoxide anion production induced by these particles was also measured. All granulocyte responses to zymosan and IgG-SRC were depressed in the three aged groups as compared to young controls. Hence, only functions involving a specific receptor (Fc or C3b receptor) seemed affected. Monocyte activity was slightly decreased in the same groups. No difference was found between AD or PD patients and normal aged subjects. Hence the phagocytic and oxidative defects we found were a consequence of aging.
PubMed: 2836744
Links to Exploration step
pubmed:2836744Le document en format XML
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<author><name sortKey="Mege, J L" sort="Mege, J L" uniqKey="Mege J" first="J L" last="Mege">J L Mege</name>
<affiliation><nlm:affiliation>Laboratoire d'Immunologie, Hôpital de Sainte-Marguerite, Marseille, France.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Capo, C" sort="Capo, C" uniqKey="Capo C" first="C" last="Capo">C. Capo</name>
</author>
<author><name sortKey="Michel, B" sort="Michel, B" uniqKey="Michel B" first="B" last="Michel">B. Michel</name>
</author>
<author><name sortKey="Gastaut, J L" sort="Gastaut, J L" uniqKey="Gastaut J" first="J L" last="Gastaut">J L Gastaut</name>
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<author><name sortKey="Bongrand, P" sort="Bongrand, P" uniqKey="Bongrand P" first="P" last="Bongrand">P. Bongrand</name>
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<author><name sortKey="Mege, J L" sort="Mege, J L" uniqKey="Mege J" first="J L" last="Mege">J L Mege</name>
<affiliation><nlm:affiliation>Laboratoire d'Immunologie, Hôpital de Sainte-Marguerite, Marseille, France.</nlm:affiliation>
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<author><name sortKey="Capo, C" sort="Capo, C" uniqKey="Capo C" first="C" last="Capo">C. Capo</name>
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<author><name sortKey="Michel, B" sort="Michel, B" uniqKey="Michel B" first="B" last="Michel">B. Michel</name>
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<author><name sortKey="Gastaut, J L" sort="Gastaut, J L" uniqKey="Gastaut J" first="J L" last="Gastaut">J L Gastaut</name>
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<author><name sortKey="Bongrand, P" sort="Bongrand, P" uniqKey="Bongrand P" first="P" last="Bongrand">P. Bongrand</name>
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<series><title level="j">Neurobiology of aging</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term>
<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Aging (metabolism)</term>
<term>Alzheimer Disease (metabolism)</term>
<term>Cytochrome c Group (metabolism)</term>
<term>Erythrocytes (metabolism)</term>
<term>Female</term>
<term>Granulocytes (metabolism)</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Monocytes (metabolism)</term>
<term>Oxidation-Reduction</term>
<term>Parkinson Disease (metabolism)</term>
<term>Phagocytosis</term>
<term>Zymosan</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytochrome c Group</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Aging</term>
<term>Alzheimer Disease</term>
<term>Erythrocytes</term>
<term>Granulocytes</term>
<term>Monocytes</term>
<term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adult</term>
<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Oxidation-Reduction</term>
<term>Phagocytosis</term>
<term>Zymosan</term>
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<front><div type="abstract" xml:lang="en">In order to study the activity of phagocytic cells in normal and pathological aging, we compared normal young and aged subjects and patients with Alzheimer's (AD) or Parkinson's (PD) disease. Blood granulocytes and monocytes were separately assayed for ingestion of three different particle species (opsonized zymosan, immunoglobulin-coated sheep red cells (IgG-SRC) and glutaraldehyde-treated sheep red cells (G-SRC]. The superoxide anion production induced by these particles was also measured. All granulocyte responses to zymosan and IgG-SRC were depressed in the three aged groups as compared to young controls. Hence, only functions involving a specific receptor (Fc or C3b receptor) seemed affected. Monocyte activity was slightly decreased in the same groups. No difference was found between AD or PD patients and normal aged subjects. Hence the phagocytic and oxidative defects we found were a consequence of aging.</div>
</front>
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<Month>06</Month>
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<DateCompleted><Year>1988</Year>
<Month>06</Month>
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<DateRevised><Year>2015</Year>
<Month>11</Month>
<Day>19</Day>
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<JournalIssue CitedMedium="Print"><Volume>9</Volume>
<Issue>2</Issue>
<PubDate><MedlineDate>1988 Mar-Apr</MedlineDate>
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<Title>Neurobiology of aging</Title>
<ISOAbbreviation>Neurobiol. Aging</ISOAbbreviation>
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<ArticleTitle>Phagocytic cell function in aged subjects.</ArticleTitle>
<Pagination><MedlinePgn>217-20</MedlinePgn>
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<Abstract><AbstractText>In order to study the activity of phagocytic cells in normal and pathological aging, we compared normal young and aged subjects and patients with Alzheimer's (AD) or Parkinson's (PD) disease. Blood granulocytes and monocytes were separately assayed for ingestion of three different particle species (opsonized zymosan, immunoglobulin-coated sheep red cells (IgG-SRC) and glutaraldehyde-treated sheep red cells (G-SRC]. The superoxide anion production induced by these particles was also measured. All granulocyte responses to zymosan and IgG-SRC were depressed in the three aged groups as compared to young controls. Hence, only functions involving a specific receptor (Fc or C3b receptor) seemed affected. Monocyte activity was slightly decreased in the same groups. No difference was found between AD or PD patients and normal aged subjects. Hence the phagocytic and oxidative defects we found were a consequence of aging.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mege</LastName>
<ForeName>J L</ForeName>
<Initials>JL</Initials>
<AffiliationInfo><Affiliation>Laboratoire d'Immunologie, Hôpital de Sainte-Marguerite, Marseille, France.</Affiliation>
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<Author ValidYN="Y"><LastName>Michel</LastName>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName>
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<MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName>
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<MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName>
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<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
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<MeshHeading><DescriptorName UI="D006098" MajorTopicYN="N">Granulocytes</DescriptorName>
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<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
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<MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName>
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<MeshHeading><DescriptorName UI="D009000" MajorTopicYN="N">Monocytes</DescriptorName>
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<MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName>
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<MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D010587" MajorTopicYN="Y">Phagocytosis</DescriptorName>
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<MeshHeading><DescriptorName UI="D015054" MajorTopicYN="N">Zymosan</DescriptorName>
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