Anti-inflammatory Therapies for Cystic Fibrosis-Related Lung Disease
Identifieur interne : 002929 ( Istex/Corpus ); précédent : 002928; suivant : 002930Anti-inflammatory Therapies for Cystic Fibrosis-Related Lung Disease
Auteurs : David P. Nichols ; Michael W. Konstan ; James F. ChmielSource :
- Clinical Reviews in Allergy & Immunology [ 1080-0549 ] ; 2008-12-01.
English descriptors
Abstract
Abstract: Cystic fibrosis (CF) is an autosomal recessive disease affecting many organ systems. In the lung, the underlying ion transport defect in CF establishes a perpetuating cycle of impaired airway clearance, chronic endobronchial infection, and exuberant inflammation. The interrelated nature of these components of CF lung disease makes it likely that the most effective therapeutic strategies will include treatments of each of these. This chapter reviews the preclinical and clinical data focused on ways to better understand and particularly to limit inflammation in the CF airway. Anti-inflammatories are an attractive therapeutic target in CF with a proven ability to decrease the rate of decline in lung function. However, the inherent complexity of the inflammatory response combined with the obvious dependency on this response to contain infection and the side effect profiles of common anti-inflammatories have made identifying the most suitable agents challenging. Research continues to discover impairments in signaling events in CF that may contribute to the excessive inflammation seen clinically. Concurrent with these findings, promising new therapies are being evaluated to determine which agents will be most effective and well tolerated. Available data from studies commenced over the last two decades, which have generated both encouraging and disappointing results, are reviewed below.
Url:
DOI: 10.1007/s12016-008-8081-2
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ISTEX:F30D95A8911972350FDACACAB2A66387CE5DEDCALe document en format XML
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Nichols</name><affiliation><mods:affiliation>Department of Pediatrics, Case Western Reserve University School of Medicine, Rainbow Babies and Children’s Hospital, Cleveland, OH, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Division of Pediatric Pulmonology, MS# 6006, Rainbow Babies and Children’s Hospital, 11100 Euclid Avenue, 44106, Cleveland, OH, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: David.Nichols@uhhospitals.org</mods:affiliation></affiliation></author><author><name sortKey="Konstan, Michael W" sort="Konstan, Michael W" uniqKey="Konstan M" first="Michael W." last="Konstan">Michael W. Konstan</name><affiliation><mods:affiliation>Department of Pediatrics, Case Western Reserve University School of Medicine, Rainbow Babies and Children’s Hospital, Cleveland, OH, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Division of Pediatric Pulmonology, MS# 6006, Rainbow Babies and Children’s Hospital, 11100 Euclid Avenue, 44106, Cleveland, OH, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: Michael.Konstan@uhhospitals.org</mods:affiliation></affiliation></author><author><name sortKey="Chmiel, James F" sort="Chmiel, James F" uniqKey="Chmiel J" first="James F." last="Chmiel">James F. Chmiel</name><affiliation><mods:affiliation>Department of Pediatrics, Case Western Reserve University School of Medicine, Rainbow Babies and Children’s Hospital, Cleveland, OH, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Division of Pediatric Pulmonology, MS# 6006, Rainbow Babies and Children’s Hospital, 11100 Euclid Avenue, 44106, Cleveland, OH, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: James.Chmiel@uhhospitals.org</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Clinical Reviews in Allergy & Immunology</title><title level="j" type="abbrev">Clinic Rev Allerg Immunol</title><idno type="ISSN">1080-0549</idno><idno type="eISSN">1559-0267</idno><imprint><publisher>Humana Press Inc</publisher><pubPlace>New York</pubPlace><date type="published" when="2008-12-01">2008-12-01</date><biblScope unit="volume">35</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="135">135</biblScope><biblScope unit="page" to="153">153</biblScope></imprint><idno type="ISSN">1080-0549</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1080-0549</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Anti-inflammatory therapy</term><term>Corticosteroids</term><term>Cystic fibrosis</term><term>Ibuprofen</term><term>Inflammation</term><term>Lung</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Cystic fibrosis (CF) is an autosomal recessive disease affecting many organ systems. In the lung, the underlying ion transport defect in CF establishes a perpetuating cycle of impaired airway clearance, chronic endobronchial infection, and exuberant inflammation. The interrelated nature of these components of CF lung disease makes it likely that the most effective therapeutic strategies will include treatments of each of these. This chapter reviews the preclinical and clinical data focused on ways to better understand and particularly to limit inflammation in the CF airway. Anti-inflammatories are an attractive therapeutic target in CF with a proven ability to decrease the rate of decline in lung function. However, the inherent complexity of the inflammatory response combined with the obvious dependency on this response to contain infection and the side effect profiles of common anti-inflammatories have made identifying the most suitable agents challenging. Research continues to discover impairments in signaling events in CF that may contribute to the excessive inflammation seen clinically. Concurrent with these findings, promising new therapies are being evaluated to determine which agents will be most effective and well tolerated. Available data from studies commenced over the last two decades, which have generated both encouraging and disappointing results, are reviewed below.</div></front></TEI><istex><corpusName>springer-journals</corpusName><author><json:item><name>David P. 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when="2008-12-01"></date><biblScope unit="volume">35</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="135">135</biblScope><biblScope unit="page" to="153">153</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2008</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Cystic fibrosis (CF) is an autosomal recessive disease affecting many organ systems. In the lung, the underlying ion transport defect in CF establishes a perpetuating cycle of impaired airway clearance, chronic endobronchial infection, and exuberant inflammation. The interrelated nature of these components of CF lung disease makes it likely that the most effective therapeutic strategies will include treatments of each of these. This chapter reviews the preclinical and clinical data focused on ways to better understand and particularly to limit inflammation in the CF airway. Anti-inflammatories are an attractive therapeutic target in CF with a proven ability to decrease the rate of decline in lung function. However, the inherent complexity of the inflammatory response combined with the obvious dependency on this response to contain infection and the side effect profiles of common anti-inflammatories have made identifying the most suitable agents challenging. Research continues to discover impairments in signaling events in CF that may contribute to the excessive inflammation seen clinically. Concurrent with these findings, promising new therapies are being evaluated to determine which agents will be most effective and well tolerated. Available data from studies commenced over the last two decades, which have generated both encouraging and disappointing results, are reviewed below.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Cystic fibrosis</term></item><item><term>Lung</term></item><item><term>Inflammation</term></item><item><term>Anti-inflammatory therapy</term></item><item><term>Corticosteroids</term></item><item><term>Ibuprofen</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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Disease</ArticleTitle><ArticleFirstPage>135</ArticleFirstPage><ArticleLastPage>153</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2008</Year><Month>4</Month><Day>17</Day></RegistrationDate><OnlineDate><Year>2008</Year><Month>6</Month><Day>11</Day></OnlineDate></ArticleHistory><ArticleCopyright><CopyrightHolderName>Humana Press Inc.</CopyrightHolderName><CopyrightYear>2008</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1 Aff2"><AuthorName DisplayOrder="Western"><GivenName>David</GivenName><GivenName>P.</GivenName><FamilyName>Nichols</FamilyName></AuthorName><Contact><Email>David.Nichols@uhhospitals.org</Email></Contact></Author><Author AffiliationIDS="Aff1 Aff2"><AuthorName DisplayOrder="Western"><GivenName>Michael</GivenName><GivenName>W.</GivenName><FamilyName>Konstan</FamilyName></AuthorName><Contact><Email>Michael.Konstan@uhhospitals.org</Email></Contact></Author><Author AffiliationIDS="Aff1 Aff2" CorrespondingAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><GivenName>James</GivenName><GivenName>F.</GivenName><FamilyName>Chmiel</FamilyName></AuthorName><Contact><Phone>+1-216-8443267</Phone><Fax>+1-216-8445916</Fax><Email>James.Chmiel@uhhospitals.org</Email></Contact></Author><Affiliation ID="Aff1"><OrgDivision>Department of Pediatrics, Case Western Reserve University School of Medicine</OrgDivision><OrgName>Rainbow Babies and Children’s Hospital</OrgName><OrgAddress><City>Cleveland</City><State>OH</State><Country Code="US">USA</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgDivision>Division of Pediatric Pulmonology, MS# 6006</OrgDivision><OrgName>Rainbow Babies and Children’s Hospital</OrgName><OrgAddress><Street>11100 Euclid Avenue</Street><City>Cleveland</City><State>OH</State><Postcode>44106</Postcode><Country Code="US">USA</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Abstract</Heading><Para>Cystic fibrosis (CF) is an autosomal recessive disease affecting many organ systems. In the lung, the underlying ion transport defect in CF establishes a perpetuating cycle of impaired airway clearance, chronic endobronchial infection, and exuberant inflammation. The interrelated nature of these components of CF lung disease makes it likely that the most effective therapeutic strategies will include treatments of each of these. This chapter reviews the preclinical and clinical data focused on ways to better understand and particularly to limit inflammation in the CF airway. Anti-inflammatories are an attractive therapeutic target in CF with a proven ability to decrease the rate of decline in lung function. However, the inherent complexity of the inflammatory response combined with the obvious dependency on this response to contain infection and the side effect profiles of common anti-inflammatories have made identifying the most suitable agents challenging. Research continues to discover impairments in signaling events in CF that may contribute to the excessive inflammation seen clinically. Concurrent with these findings, promising new therapies are being evaluated to determine which agents will be most effective and well tolerated. Available data from studies commenced over the last two decades, which have generated both encouraging and disappointing results, are reviewed below.</Para></Abstract><KeywordGroup Language="En"><Heading>Keywords</Heading><Keyword>Cystic fibrosis</Keyword><Keyword>Lung</Keyword><Keyword>Inflammation</Keyword><Keyword>Anti-inflammatory therapy</Keyword><Keyword>Corticosteroids</Keyword><Keyword>Ibuprofen</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Anti-inflammatory Therapies for Cystic Fibrosis-Related Lung Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Anti-inflammatory Therapies for Cystic Fibrosis-Related Lung Disease</title></titleInfo><name type="personal"><namePart type="given">David</namePart><namePart type="given">P.</namePart><namePart type="family">Nichols</namePart><affiliation>Department of Pediatrics, Case Western Reserve University School of Medicine, Rainbow Babies and Children’s Hospital, Cleveland, OH, USA</affiliation><affiliation>Division of Pediatric Pulmonology, MS# 6006, Rainbow Babies and Children’s Hospital, 11100 Euclid Avenue, 44106, Cleveland, OH, USA</affiliation><affiliation>E-mail: David.Nichols@uhhospitals.org</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael</namePart><namePart type="given">W.</namePart><namePart type="family">Konstan</namePart><affiliation>Department of Pediatrics, Case Western Reserve University School of Medicine, Rainbow Babies and Children’s Hospital, Cleveland, OH, USA</affiliation><affiliation>Division of Pediatric Pulmonology, MS# 6006, Rainbow Babies and Children’s Hospital, 11100 Euclid Avenue, 44106, Cleveland, OH, USA</affiliation><affiliation>E-mail: Michael.Konstan@uhhospitals.org</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">James</namePart><namePart type="given">F.</namePart><namePart type="family">Chmiel</namePart><affiliation>Department of Pediatrics, Case Western Reserve University School of Medicine, Rainbow Babies and Children’s Hospital, Cleveland, OH, USA</affiliation><affiliation>Division of Pediatric Pulmonology, MS# 6006, Rainbow Babies and Children’s Hospital, 11100 Euclid Avenue, 44106, Cleveland, OH, USA</affiliation><affiliation>E-mail: James.Chmiel@uhhospitals.org</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">2008-12-01</dateIssued><copyrightDate encoding="w3cdtf">2008</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Abstract: Cystic fibrosis (CF) is an autosomal recessive disease affecting many organ systems. In the lung, the underlying ion transport defect in CF establishes a perpetuating cycle of impaired airway clearance, chronic endobronchial infection, and exuberant inflammation. The interrelated nature of these components of CF lung disease makes it likely that the most effective therapeutic strategies will include treatments of each of these. This chapter reviews the preclinical and clinical data focused on ways to better understand and particularly to limit inflammation in the CF airway. Anti-inflammatories are an attractive therapeutic target in CF with a proven ability to decrease the rate of decline in lung function. However, the inherent complexity of the inflammatory response combined with the obvious dependency on this response to contain infection and the side effect profiles of common anti-inflammatories have made identifying the most suitable agents challenging. Research continues to discover impairments in signaling events in CF that may contribute to the excessive inflammation seen clinically. Concurrent with these findings, promising new therapies are being evaluated to determine which agents will be most effective and well tolerated. Available data from studies commenced over the last two decades, which have generated both encouraging and disappointing results, are reviewed below.</abstract><subject lang="en"><genre>Keywords</genre><topic>Cystic fibrosis</topic><topic>Lung</topic><topic>Inflammation</topic><topic>Anti-inflammatory therapy</topic><topic>Corticosteroids</topic><topic>Ibuprofen</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">2008-10-22</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">8</identifier><identifier type="VolumeIssueCount">3</identifier><part><date>2008</date><detail type="volume"><number>35</number><caption>vol.</caption></detail><detail type="issue"><number>3</number><caption>no.</caption></detail><extent unit="pages"><start>135</start><end>153</end></extent></part><recordInfo><recordOrigin>Humana Press Inc., 2008</recordOrigin></recordInfo></relatedItem><identifier type="istex">F30D95A8911972350FDACACAB2A66387CE5DEDCA</identifier><identifier type="ark">ark:/67375/VQC-5345R921-N</identifier><identifier type="DOI">10.1007/s12016-008-8081-2</identifier><identifier type="ArticleID">8081</identifier><identifier type="ArticleID">s12016-008-8081-2</identifier><accessCondition type="use and reproduction" contentType="copyright">Humana Press Inc., 2008</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., 2008</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-5345R921-N/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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