Infections and Autoimmunity: A Panorama
Identifieur interne : 000845 ( Istex/Corpus ); précédent : 000844; suivant : 000846Infections and Autoimmunity: A Panorama
Auteurs : V. Pordeus ; M. Szyper-Kravitz ; R. A. Levy ; N. M. Vaz ; Y. ShoenfeldSource :
- Clinical Reviews in Allergy & Immunology [ 1080-0549 ] ; 2008-06-01.
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- KwdEn :
Abstract
Abstract: For more than 2,000 years, it was thought that malignant spirits caused diseases. By the end of nineteenth century, these beliefs were displaced by more modern concepts of disease, namely, the formulation of the “germ theory,” which asserted that bacteria or other microorganisms caused disease. With the emergence of chronic degenerative and of autoimmune diseases in the last century, the causative role of microorganisms has been intensely debated; however, no clear explanatory models have been achieved. In this review, we examine the current available literature regarding the relationships between infections and 16 autoimmune diseases. We critically analyzed clinical, serological, and molecular associations, and reviewed experimental models of induction of and, alternatively, protection from autoimmune diseases by infection. After reviewing several studies and reports, a clinical and experimental pattern emerges: Chronic and multiple infections with viruses, such as Epstein–Barr virus and cytomegalovirus, and bacteria, such as H. pylori, may, in susceptible individuals, play a role in the evolvement of autoimmune diseases. As the vast majority of infections pertain to our resident microbiota and endogenous retroviruses and healthy carriage of infections is the rule, we propose to focus on understanding the mechanisms of this healthy carrier state and what changes its configurations to infectious syndromes, to the restoration of health, or to the sustaining of illness into a chronic state and/or autoimmune disease. It seems that in the development of this healthy carriage state, the infection or colonization in early stages of ontogenesis with key microorganisms, also called ‘old friends’ (lactobacilli, bifidobacteria among others), are important for the healthy living and for the protection from infectious and autoimmune syndromes.
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DOI: 10.1007/s12016-007-8048-8
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By the end of nineteenth century, these beliefs were displaced by more modern concepts of disease, namely, the formulation of the “germ theory,” which asserted that bacteria or other microorganisms caused disease. With the emergence of chronic degenerative and of autoimmune diseases in the last century, the causative role of microorganisms has been intensely debated; however, no clear explanatory models have been achieved. In this review, we examine the current available literature regarding the relationships between infections and 16 autoimmune diseases. We critically analyzed clinical, serological, and molecular associations, and reviewed experimental models of induction of and, alternatively, protection from autoimmune diseases by infection. After reviewing several studies and reports, a clinical and experimental pattern emerges: Chronic and multiple infections with viruses, such as Epstein–Barr virus and cytomegalovirus, and bacteria, such as H. pylori, may, in susceptible individuals, play a role in the evolvement of autoimmune diseases. As the vast majority of infections pertain to our resident microbiota and endogenous retroviruses and healthy carriage of infections is the rule, we propose to focus on understanding the mechanisms of this healthy carrier state and what changes its configurations to infectious syndromes, to the restoration of health, or to the sustaining of illness into a chronic state and/or autoimmune disease. It seems that in the development of this healthy carriage state, the infection or colonization in early stages of ontogenesis with key microorganisms, also called ‘old friends’ (lactobacilli, bifidobacteria among others), are important for the healthy living and for the protection from infectious and autoimmune syndromes.</div></front></TEI><istex><corpusName>springer-journals</corpusName><author><json:item><name>V. Pordeus</name><affiliations><json:string>Clinical Research, Pro Cardiaco Hospital Research Center—PROCEP, Rio de Janeiro, Brazil</json:string><json:string>Center for Autoimmune diseases, Department of Medicine B, Sheba Medical Center, Tel Hashomer, Israel</json:string></affiliations></json:item><json:item><name>M. Szyper-Kravitz</name><affiliations><json:string>Center for Autoimmune diseases, Department of Medicine B, Sheba Medical Center, Tel Hashomer, Israel</json:string></affiliations></json:item><json:item><name>R. A. 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By the end of nineteenth century, these beliefs were displaced by more modern concepts of disease, namely, the formulation of the “germ theory,” which asserted that bacteria or other microorganisms caused disease. With the emergence of chronic degenerative and of autoimmune diseases in the last century, the causative role of microorganisms has been intensely debated; however, no clear explanatory models have been achieved. In this review, we examine the current available literature regarding the relationships between infections and 16 autoimmune diseases. We critically analyzed clinical, serological, and molecular associations, and reviewed experimental models of induction of and, alternatively, protection from autoimmune diseases by infection. After reviewing several studies and reports, a clinical and experimental pattern emerges: Chronic and multiple infections with viruses, such as Epstein–Barr virus and cytomegalovirus, and bacteria, such as H. pylori, may, in susceptible individuals, play a role in the evolvement of autoimmune diseases. As the vast majority of infections pertain to our resident microbiota and endogenous retroviruses and healthy carriage of infections is the rule, we propose to focus on understanding the mechanisms of this healthy carrier state and what changes its configurations to infectious syndromes, to the restoration of health, or to the sustaining of illness into a chronic state and/or autoimmune disease. 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By the end of nineteenth century, these beliefs were displaced by more modern concepts of disease, namely, the formulation of the “germ theory,” which asserted that bacteria or other microorganisms caused disease. With the emergence of chronic degenerative and of autoimmune diseases in the last century, the causative role of microorganisms has been intensely debated; however, no clear explanatory models have been achieved. In this review, we examine the current available literature regarding the relationships between infections and 16 autoimmune diseases. We critically analyzed clinical, serological, and molecular associations, and reviewed experimental models of induction of and, alternatively, protection from autoimmune diseases by infection. After reviewing several studies and reports, a clinical and experimental pattern emerges: Chronic and multiple infections with viruses, such as Epstein–Barr virus and cytomegalovirus, and bacteria, such as H. pylori, may, in susceptible individuals, play a role in the evolvement of autoimmune diseases. As the vast majority of infections pertain to our resident microbiota and endogenous retroviruses and healthy carriage of infections is the rule, we propose to focus on understanding the mechanisms of this healthy carrier state and what changes its configurations to infectious syndromes, to the restoration of health, or to the sustaining of illness into a chronic state and/or autoimmune disease. It seems that in the development of this healthy carriage state, the infection or colonization in early stages of ontogenesis with key microorganisms, also called ‘old friends’ (lactobacilli, bifidobacteria among others), are important for the healthy living and for the protection from infectious and autoimmune syndromes.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Infections</term></item><item><term>Autoimmune diseases</term></item><item><term>Chronic infection</term></item><item><term>Multiple infections</term></item><item><term>Old friends</term></item><item><term>Healthy carriage</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Medicine & Public Health</head><item><term>Internal Medicine</term></item><item><term>Immunology</term></item><item><term>Allergology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change 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DisplayOrder="Western"><GivenName>M.</GivenName><FamilyName>Szyper-Kravitz</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2"><AuthorName DisplayOrder="Western"><GivenName>R.</GivenName><GivenName>A.</GivenName><FamilyName>Levy</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff3"><AuthorName DisplayOrder="Western"><GivenName>N.</GivenName><GivenName>M.</GivenName><FamilyName>Vaz</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff4" CorrespondingAffiliationID="Aff4"><AuthorName DisplayOrder="Western"><GivenName>Y.</GivenName><FamilyName>Shoenfeld</FamilyName></AuthorName><Contact><Email>shoenfel@post.tau.ac.il</Email></Contact></Author><Affiliation ID="Aff1"><OrgDivision>Clinical Research</OrgDivision><OrgName>Pro Cardiaco Hospital Research Center—PROCEP</OrgName><OrgAddress><City>Rio de Janeiro</City><Country Code="BR">Brazil</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgDivision>Rheumatology Discipline, Faculty of Medicine</OrgDivision><OrgName>Universidade do Estado do Rio de Janeiro</OrgName><OrgAddress><City>Rio de Janeiro</City><State>RJ</State><Country Code="BR">Brazil</Country></OrgAddress></Affiliation><Affiliation ID="Aff3"><OrgDivision>Department of Immunology and Biochemistry–ICB</OrgDivision><OrgName>Universidade Federal de Minas Gerais</OrgName><OrgAddress><City>Belo Horizonte</City><Country Code="BR">Brazil</Country></OrgAddress></Affiliation><Affiliation ID="Aff4"><OrgDivision>Center for Autoimmune diseases, Department of Medicine B</OrgDivision><OrgName>Sheba Medical Center</OrgName><OrgAddress><City>Tel Hashomer</City><Country Code="IL">Israel</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Abstract</Heading><Para>For more than 2,000 years, it was thought that malignant spirits caused diseases. By the end of nineteenth century, these beliefs were displaced by more modern concepts of disease, namely, the formulation of the “germ theory,” which asserted that bacteria or other microorganisms caused disease. With the emergence of chronic degenerative and of autoimmune diseases in the last century, the causative role of microorganisms has been intensely debated; however, no clear explanatory models have been achieved. In this review, we examine the current available literature regarding the relationships between infections and 16 autoimmune diseases. We critically analyzed clinical, serological, and molecular associations, and reviewed experimental models of induction of and, alternatively, protection from autoimmune diseases by infection. After reviewing several studies and reports, a clinical and experimental pattern emerges: Chronic and multiple infections with viruses, such as Epstein–Barr virus and cytomegalovirus, and bacteria, such as <Emphasis Type="Italic">H. pylori</Emphasis>, may, in susceptible individuals, play a role in the evolvement of autoimmune diseases. As the vast majority of infections pertain to our resident microbiota and endogenous retroviruses and healthy carriage of infections is the rule, we propose to focus on understanding the mechanisms of this healthy carrier state and what changes its configurations to infectious syndromes, to the restoration of health, or to the sustaining of illness into a chronic state and/or autoimmune disease. It seems that in the development of this healthy carriage state, the infection or colonization in early stages of ontogenesis with key microorganisms, also called ‘old friends’ (lactobacilli, bifidobacteria among others), are important for the healthy living and for the protection from infectious and autoimmune syndromes.</Para></Abstract><KeywordGroup Language="En"><Heading>Keywords</Heading><Keyword>Infections</Keyword><Keyword>Autoimmune diseases</Keyword><Keyword>Chronic infection</Keyword><Keyword>Multiple infections</Keyword><Keyword>Old friends</Keyword><Keyword>Healthy carriage</Keyword></KeywordGroup><ArticleNote Type="Misc"><SimplePara>This study was supported by the Wilhelm Agricola Research Grant, Federico Foundation, Zurich, Switzerland.</SimplePara></ArticleNote></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Infections and Autoimmunity: A Panorama</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Infections and Autoimmunity: A Panorama</title></titleInfo><name type="personal"><namePart type="given">V.</namePart><namePart type="family">Pordeus</namePart><affiliation>Clinical Research, Pro Cardiaco Hospital Research Center—PROCEP, Rio de Janeiro, Brazil</affiliation><affiliation>Center for Autoimmune diseases, Department of Medicine B, Sheba Medical Center, Tel Hashomer, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Szyper-Kravitz</namePart><affiliation>Center for Autoimmune diseases, Department of Medicine B, Sheba Medical Center, Tel Hashomer, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.</namePart><namePart type="given">A.</namePart><namePart type="family">Levy</namePart><affiliation>Rheumatology Discipline, Faculty of Medicine, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ, Brazil</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N.</namePart><namePart type="given">M.</namePart><namePart type="family">Vaz</namePart><affiliation>Department of Immunology and Biochemistry–ICB, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">Y.</namePart><namePart type="family">Shoenfeld</namePart><affiliation>Center for Autoimmune diseases, Department of Medicine B, Sheba Medical Center, Tel Hashomer, Israel</affiliation><affiliation>E-mail: shoenfel@post.tau.ac.il</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>Humana Press Inc</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2008-06-01</dateIssued><copyrightDate encoding="w3cdtf">2007</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Abstract: For more than 2,000 years, it was thought that malignant spirits caused diseases. By the end of nineteenth century, these beliefs were displaced by more modern concepts of disease, namely, the formulation of the “germ theory,” which asserted that bacteria or other microorganisms caused disease. With the emergence of chronic degenerative and of autoimmune diseases in the last century, the causative role of microorganisms has been intensely debated; however, no clear explanatory models have been achieved. In this review, we examine the current available literature regarding the relationships between infections and 16 autoimmune diseases. We critically analyzed clinical, serological, and molecular associations, and reviewed experimental models of induction of and, alternatively, protection from autoimmune diseases by infection. After reviewing several studies and reports, a clinical and experimental pattern emerges: Chronic and multiple infections with viruses, such as Epstein–Barr virus and cytomegalovirus, and bacteria, such as H. pylori, may, in susceptible individuals, play a role in the evolvement of autoimmune diseases. As the vast majority of infections pertain to our resident microbiota and endogenous retroviruses and healthy carriage of infections is the rule, we propose to focus on understanding the mechanisms of this healthy carrier state and what changes its configurations to infectious syndromes, to the restoration of health, or to the sustaining of illness into a chronic state and/or autoimmune disease. It seems that in the development of this healthy carriage state, the infection or colonization in early stages of ontogenesis with key microorganisms, also called ‘old friends’ (lactobacilli, bifidobacteria among others), are important for the healthy living and for the protection from infectious and autoimmune syndromes.</abstract><subject lang="en"><genre>Keywords</genre><topic>Infections</topic><topic>Autoimmune diseases</topic><topic>Chronic infection</topic><topic>Multiple infections</topic><topic>Old friends</topic><topic>Healthy carriage</topic></subject><relatedItem type="host"><titleInfo><title>Clinical Reviews in Allergy & Immunology</title></titleInfo><titleInfo type="abbreviated"><title>Clinic Rev Allerg Immunol</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>Springer</publisher><dateIssued encoding="w3cdtf">2008-05-22</dateIssued><copyrightDate encoding="w3cdtf">2008</copyrightDate></originInfo><subject><genre>Medicine & Public Health</genre><topic>Internal Medicine</topic><topic>Immunology</topic><topic>Allergology</topic></subject><identifier type="ISSN">1080-0549</identifier><identifier type="eISSN">1559-0267</identifier><identifier type="JournalID">12016</identifier><identifier type="IssueArticleCount">18</identifier><identifier type="VolumeIssueCount">1</identifier><part><date>2008</date><detail type="volume"><number>34</number><caption>vol.</caption></detail><detail type="issue"><number>3</number><caption>no.</caption></detail><extent unit="pages"><start>283</start><end>299</end></extent></part><recordInfo><recordOrigin>Humana Press, 2008</recordOrigin></recordInfo></relatedItem><identifier type="istex">0AA296BA12B51B81A6255076077CCCD6854ACD84</identifier><identifier type="ark">ark:/67375/VQC-CFBKK05Q-P</identifier><identifier type="DOI">10.1007/s12016-007-8048-8</identifier><identifier type="ArticleID">8048</identifier><identifier type="ArticleID">s12016-007-8048-8</identifier><accessCondition type="use and reproduction" contentType="copyright">Humana Press Inc., 2007</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</recordContentSource><recordOrigin>Humana Press Inc., 2007</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-CFBKK05Q-P/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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