Innate immunity, local inflammation, and degenerative disease.
Identifieur interne : 001499 ( PubMed/Corpus ); précédent : 001498; suivant : 001500Innate immunity, local inflammation, and degenerative disease.
Auteurs : Patrick L. Mcgeer ; Edith G. McgeerSource :
- Science of aging knowledge environment : SAGE KE [ 1539-6150 ] ; 2002.
English descriptors
- KwdEn :
- Alzheimer Disease (immunology), Alzheimer Disease (metabolism), Alzheimer Disease (pathology), Alzheimer Disease (prevention & control), Animals, Anti-Inflammatory Agents, Non-Steroidal (therapeutic use), Humans, Immunity, Innate (immunology), Inflammation (immunology), Inflammation (metabolism), Inflammation (pathology), Inflammation Mediators (immunology), Inflammation Mediators (metabolism), Parkinson Disease (immunology), Parkinson Disease (metabolism), Parkinson Disease (prevention & control).
- MESH :
- chemical , immunology : Inflammation Mediators.
- chemical , metabolism : Inflammation Mediators.
- chemical , therapeutic use : Anti-Inflammatory Agents, Non-Steroidal.
- immunology : Alzheimer Disease, Immunity, Innate, Inflammation, Parkinson Disease.
- metabolism : Alzheimer Disease, Inflammation, Parkinson Disease.
- pathology : Alzheimer Disease, Inflammation.
- prevention & control : Alzheimer Disease, Parkinson Disease.
- Animals, Humans.
Abstract
The brain lesions associated with Alzheimer's disease (AD), which are referred to as neurofibrillary tangles and senile plaques, are characterized by the presence of a broad spectrum of inflammatory mediators. Surprisingly, these mediators, which include complement proteins, inflammatory cytokines, prostaglandins, and acute phase reactants such as C-reactive protein and amyloid P, are produced by resident brain cells, including neurons. Although secondary to the fundamental pathology caused by the presence of tangles and plaques, there is strong evidence that inflammation exacerbates the neuronal loss. In particular, AD lesions show evidence of self-attack by the complement system--a part of the immune system that normally functions to rid the body of invading pathogens. However, the lesions are devoid of significant T cell infiltration, a hallmark of an inflammatory immune response, and antibodies. We define this phenomenon as autotoxicity to distinguish it from classical autoimmunity, in which the body raises antibodies to normal endogenous macromolecules. Locally produced inflammatory mediators have also been identified in atherosclerotic plaques, along with evidence of complement self-attack. As was previously shown for heart attacks, epidemiological evidence indicates that extended use of nonsteroidal anti-inflammatory drugs (NSAIDs) results in a reduced risk of AD. NSAIDs inhibit the production of prostaglandin inflammatory mediators, but powerful new therapeutic agents might be developed by targeting more critical inflammatory mechanisms, especially the complement system.
DOI: 10.1126/sageke.2002.29.re3
PubMed: 14602998
Links to Exploration step
pubmed:14602998Le document en format XML
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Mcgeer</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:14602998</idno><idno type="pmid">14602998</idno><idno type="doi">10.1126/sageke.2002.29.re3</idno><idno type="wicri:Area/PubMed/Corpus">001499</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001499</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Innate immunity, local inflammation, and degenerative disease.</title><author><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L" last="Mcgeer">Patrick L. Mcgeer</name><affiliation><nlm:affiliation>Kinsmen Laboratory of Neurological Research at the University of British Columbia, Vancouver, BC, V6T 1Z3, Canada. mcgeerpl@interchange.ubc.ca</nlm:affiliation></affiliation></author><author><name sortKey="Mcgeer, Edith G" sort="Mcgeer, Edith G" uniqKey="Mcgeer E" first="Edith G" last="Mcgeer">Edith G. 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Surprisingly, these mediators, which include complement proteins, inflammatory cytokines, prostaglandins, and acute phase reactants such as C-reactive protein and amyloid P, are produced by resident brain cells, including neurons. Although secondary to the fundamental pathology caused by the presence of tangles and plaques, there is strong evidence that inflammation exacerbates the neuronal loss. In particular, AD lesions show evidence of self-attack by the complement system--a part of the immune system that normally functions to rid the body of invading pathogens. However, the lesions are devoid of significant T cell infiltration, a hallmark of an inflammatory immune response, and antibodies. We define this phenomenon as autotoxicity to distinguish it from classical autoimmunity, in which the body raises antibodies to normal endogenous macromolecules. Locally produced inflammatory mediators have also been identified in atherosclerotic plaques, along with evidence of complement self-attack. As was previously shown for heart attacks, epidemiological evidence indicates that extended use of nonsteroidal anti-inflammatory drugs (NSAIDs) results in a reduced risk of AD. NSAIDs inhibit the production of prostaglandin inflammatory mediators, but powerful new therapeutic agents might be developed by targeting more critical inflammatory mechanisms, especially the complement system.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">14602998</PMID><DateCreated><Year>2003</Year><Month>11</Month><Day>06</Day></DateCreated><DateCompleted><Year>2003</Year><Month>11</Month><Day>07</Day></DateCompleted><DateRevised><Year>2008</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1539-6150</ISSN><JournalIssue CitedMedium="Internet"><Volume>2002</Volume><Issue>29</Issue><PubDate><Year>2002</Year><Month>Jul</Month><Day>24</Day></PubDate></JournalIssue><Title>Science of aging knowledge environment : SAGE KE</Title><ISOAbbreviation>Sci Aging Knowledge Environ</ISOAbbreviation></Journal><ArticleTitle>Innate immunity, local inflammation, and degenerative disease.</ArticleTitle><Pagination><MedlinePgn>re3</MedlinePgn></Pagination><Abstract><AbstractText>The brain lesions associated with Alzheimer's disease (AD), which are referred to as neurofibrillary tangles and senile plaques, are characterized by the presence of a broad spectrum of inflammatory mediators. Surprisingly, these mediators, which include complement proteins, inflammatory cytokines, prostaglandins, and acute phase reactants such as C-reactive protein and amyloid P, are produced by resident brain cells, including neurons. Although secondary to the fundamental pathology caused by the presence of tangles and plaques, there is strong evidence that inflammation exacerbates the neuronal loss. In particular, AD lesions show evidence of self-attack by the complement system--a part of the immune system that normally functions to rid the body of invading pathogens. However, the lesions are devoid of significant T cell infiltration, a hallmark of an inflammatory immune response, and antibodies. We define this phenomenon as autotoxicity to distinguish it from classical autoimmunity, in which the body raises antibodies to normal endogenous macromolecules. Locally produced inflammatory mediators have also been identified in atherosclerotic plaques, along with evidence of complement self-attack. As was previously shown for heart attacks, epidemiological evidence indicates that extended use of nonsteroidal anti-inflammatory drugs (NSAIDs) results in a reduced risk of AD. NSAIDs inhibit the production of prostaglandin inflammatory mediators, but powerful new therapeutic agents might be developed by targeting more critical inflammatory mechanisms, especially the complement system.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>McGeer</LastName><ForeName>Patrick L</ForeName><Initials>PL</Initials><AffiliationInfo><Affiliation>Kinsmen Laboratory of Neurological Research at the University of British Columbia, Vancouver, BC, V6T 1Z3, Canada. mcgeerpl@interchange.ubc.ca</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McGeer</LastName><ForeName>Edith G</ForeName><Initials>EG</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2002</Year><Month>07</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Sci Aging Knowledge Environ</MedlineTA><NlmUniqueID>101146039</NlmUniqueID><ISSNLinking>1539-6150</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000894">Anti-Inflammatory Agents, Non-Steroidal</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018836">Inflammation Mediators</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000544" MajorTopicYN="N">Alzheimer Disease</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000894" MajorTopicYN="N">Anti-Inflammatory Agents, Non-Steroidal</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007113" MajorTopicYN="N">Immunity, Innate</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018836" MajorTopicYN="N">Inflammation Mediators</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>91</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2003</Year><Month>11</Month><Day>7</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2003</Year><Month>11</Month><Day>7</Day><Hour>5</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2003</Year><Month>11</Month><Day>7</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">14602998</ArticleId><ArticleId IdType="doi">10.1126/sageke.2002.29.re3</ArticleId><ArticleId IdType="pii">2002/29/re3</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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