Novel therapeutic targets for inflammatory bowel disease.
Identifieur interne : 000C42 ( Main/Exploration ); précédent : 000C41; suivant : 000C43Novel therapeutic targets for inflammatory bowel disease.
Auteurs : Marjorie Argollo [Brésil] ; Gionata Fiorino [Italie] ; Pieter Hindryckx [Belgique] ; Laurent Peyrin-Biroulet [France] ; Silvio Danese [Italie]Source :
- Journal of autoimmunity [ 1095-9157 ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Anti-inflammatoires (pharmacologie), Anti-inflammatoires (usage thérapeutique), Facteur de nécrose tumorale alpha (métabolisme), Humains (MeSH), Inflammation (traitement médicamenteux), Maladies inflammatoires intestinales (métabolisme), Maladies inflammatoires intestinales (traitement médicamenteux), Transduction du signal (effets des médicaments et des substances chimiques).
- MESH :
- effets des médicaments et des substances chimiques : Transduction du signal.
- métabolisme : Facteur de nécrose tumorale alpha, Maladies inflammatoires intestinales.
- pharmacologie : Anti-inflammatoires.
- traitement médicamenteux : Inflammation, Maladies inflammatoires intestinales.
- usage thérapeutique : Anti-inflammatoires.
- Animaux, Humains.
English descriptors
- KwdEn :
- Animals (MeSH), Anti-Inflammatory Agents (pharmacology), Anti-Inflammatory Agents (therapeutic use), Humans (MeSH), Inflammation (drug therapy), Inflammatory Bowel Diseases (drug therapy), Inflammatory Bowel Diseases (metabolism), Signal Transduction (drug effects), Tumor Necrosis Factor-alpha (metabolism).
- MESH :
- chemical , metabolism : Tumor Necrosis Factor-alpha.
- chemical , pharmacology : Anti-Inflammatory Agents.
- chemical , therapeutic use : Anti-Inflammatory Agents.
- drug effects : Signal Transduction.
- drug therapy : Inflammation, Inflammatory Bowel Diseases.
- metabolism : Inflammatory Bowel Diseases.
- Animals, Humans.
Abstract
Inflammatory bowel disease (IBD), including Crohn's disease (CD) and Ulcerative Colitis (UC), are immune mediated conditions associated with progressive damage of the inflamed gut tissue, and have a considerable impact on the patient's quality of life. The pathogenesis remains uncertain, but it is clear that complex mechanisms associated with host and luminal factors are involved, generating an unbalance between pro- and anti-inflammatory signaling. It is well established that the purpose of an adequate and complete control of the intestinal inflammation measured not only by clinical symptoms, but also with more objective data such as fecal biomarkers (calprotectin) and endoscopy. The treat to target approach possibly correlates with minor risk for complications associated with IBD, specially surgery and cancer. The most studied inflammatory pathway in IBD, is described to be dependent of the pro-inflammatory cytokine tumor necrosis factor-alfa (TNF-α), and compose the first line studies for development of biological drugs, in this case, targeting specifically the action of TNF-α. Even though, the use of anti-TNFs drugs are associated with improvement of the inflammation in some patients, a great portion do not respond at first or lose response over time. These findings made clear about the possibility of other mechanisms involved in perpetuating the chronic inflammatory state. Many years of intensive research have led to the identification of different inflammatory pathways that form the basis of the intensive drug development that we are experiencing today. These novel drugs include agents that target leukocyte trafficking, Interleukin (IL) 23, Janus kinases (JAK), Sphingosine 1 phosphate (S1P) and Smad7, an inhibitor of the immunosuppressive cytokine transforming growth factor β1 (TGF-β1). In this manuscript, we aim to review the most promising late-stage drug candidates for the treatment of IBD.
DOI: 10.1016/j.jaut.2017.07.004
PubMed: 28711286
Affiliations:
- Belgique, Brésil, France, Italie
- Lombardie, Lorraine (région), État de São Paulo
- Milan, Nancy, São Paulo
- Centre hospitalier régional et universitaire de Nancy, Université de Lorraine
Links toward previous steps (curation, corpus...)
Le document en format XML
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The pathogenesis remains uncertain, but it is clear that complex mechanisms associated with host and luminal factors are involved, generating an unbalance between pro- and anti-inflammatory signaling. It is well established that the purpose of an adequate and complete control of the intestinal inflammation measured not only by clinical symptoms, but also with more objective data such as fecal biomarkers (calprotectin) and endoscopy. The treat to target approach possibly correlates with minor risk for complications associated with IBD, specially surgery and cancer. The most studied inflammatory pathway in IBD, is described to be dependent of the pro-inflammatory cytokine tumor necrosis factor-alfa (TNF-α), and compose the first line studies for development of biological drugs, in this case, targeting specifically the action of TNF-α. Even though, the use of anti-TNFs drugs are associated with improvement of the inflammation in some patients, a great portion do not respond at first or lose response over time. These findings made clear about the possibility of other mechanisms involved in perpetuating the chronic inflammatory state. Many years of intensive research have led to the identification of different inflammatory pathways that form the basis of the intensive drug development that we are experiencing today. These novel drugs include agents that target leukocyte trafficking, Interleukin (IL) 23, Janus kinases (JAK), Sphingosine 1 phosphate (S1P) and Smad7, an inhibitor of the immunosuppressive cytokine transforming growth factor β1 (TGF-β1). In this manuscript, we aim to review the most promising late-stage drug candidates for the treatment of IBD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28711286</PMID><DateCompleted><Year>2018</Year><Month>02</Month><Day>05</Day></DateCompleted><DateRevised><Year>2018</Year><Month>02</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1095-9157</ISSN><JournalIssue CitedMedium="Internet"><Volume>85</Volume><PubDate><Year>2017</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Journal of autoimmunity</Title><ISOAbbreviation>J Autoimmun</ISOAbbreviation></Journal><ArticleTitle>Novel therapeutic targets for inflammatory bowel disease.</ArticleTitle><Pagination><MedlinePgn>103-116</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0896-8411(17)30421-3</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jaut.2017.07.004</ELocationID><Abstract><AbstractText>Inflammatory bowel disease (IBD), including Crohn's disease (CD) and Ulcerative Colitis (UC), are immune mediated conditions associated with progressive damage of the inflamed gut tissue, and have a considerable impact on the patient's quality of life. The pathogenesis remains uncertain, but it is clear that complex mechanisms associated with host and luminal factors are involved, generating an unbalance between pro- and anti-inflammatory signaling. It is well established that the purpose of an adequate and complete control of the intestinal inflammation measured not only by clinical symptoms, but also with more objective data such as fecal biomarkers (calprotectin) and endoscopy. The treat to target approach possibly correlates with minor risk for complications associated with IBD, specially surgery and cancer. The most studied inflammatory pathway in IBD, is described to be dependent of the pro-inflammatory cytokine tumor necrosis factor-alfa (TNF-α), and compose the first line studies for development of biological drugs, in this case, targeting specifically the action of TNF-α. Even though, the use of anti-TNFs drugs are associated with improvement of the inflammation in some patients, a great portion do not respond at first or lose response over time. These findings made clear about the possibility of other mechanisms involved in perpetuating the chronic inflammatory state. Many years of intensive research have led to the identification of different inflammatory pathways that form the basis of the intensive drug development that we are experiencing today. These novel drugs include agents that target leukocyte trafficking, Interleukin (IL) 23, Janus kinases (JAK), Sphingosine 1 phosphate (S1P) and Smad7, an inhibitor of the immunosuppressive cytokine transforming growth factor β1 (TGF-β1). In this manuscript, we aim to review the most promising late-stage drug candidates for the treatment of IBD.</AbstractText><CopyrightInformation>Copyright © 2017. Published by Elsevier Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Argollo</LastName><ForeName>Marjorie</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Gastroenterology, Universidade Federal de São Paulo, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fiorino</LastName><ForeName>Gionata</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>IBD Center, Department of Gastroenterology, Humanitas Research Hospital, Rozzano, Milan, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hindryckx</LastName><ForeName>Pieter</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Gastroenterology, University Hospital of Ghent, Ghent, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Peyrin-Biroulet</LastName><ForeName>Laurent</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Gastroenterology and Inserm U954, Nancy University Hospital, Lorraine University, Vandoeuvre, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Danese</LastName><ForeName>Silvio</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>IBD Center, Department of Gastroenterology, Humanitas Research Hospital, Rozzano, Milan, Italy; Department of Biomedical Sciences, Humanitas University, Rozzano, Milan, Italy. Electronic address: sdanese@hotmail.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>07</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Autoimmun</MedlineTA><NlmUniqueID>8812164</NlmUniqueID><ISSNLinking>0896-8411</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000893">Anti-Inflammatory Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000893" MajorTopicYN="N">Anti-Inflammatory Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015212" MajorTopicYN="N">Inflammatory Bowel Diseases</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014409" MajorTopicYN="N">Tumor Necrosis Factor-alpha</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Anti-adhesion molecules</Keyword><Keyword MajorTopicYN="N">Anti-cytokine</Keyword><Keyword MajorTopicYN="N">Biologics</Keyword><Keyword MajorTopicYN="N">Inflammatory bowel disease</Keyword><Keyword MajorTopicYN="N">Small molecules drugs</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>06</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2017</Year><Month>07</Month><Day>03</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>07</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>7</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2018</Year><Month>2</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>7</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28711286</ArticleId><ArticleId IdType="pii">S0896-8411(17)30421-3</ArticleId><ArticleId IdType="doi">10.1016/j.jaut.2017.07.004</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Belgique</li><li>Brésil</li><li>France</li><li>Italie</li></country><region><li>Lombardie</li><li>Lorraine (région)</li><li>État de São Paulo</li></region><settlement><li>Milan</li><li>Nancy</li><li>São Paulo</li></settlement><orgName><li>Centre hospitalier régional et universitaire de Nancy</li><li>Université de Lorraine</li></orgName></list><tree><country name="Brésil"><region name="État de São Paulo"><name sortKey="Argollo, Marjorie" sort="Argollo, Marjorie" uniqKey="Argollo M" first="Marjorie" last="Argollo">Marjorie Argollo</name></region></country><country name="Italie"><region name="Lombardie"><name sortKey="Fiorino, Gionata" sort="Fiorino, Gionata" uniqKey="Fiorino G" first="Gionata" last="Fiorino">Gionata Fiorino</name></region><name sortKey="Danese, Silvio" sort="Danese, Silvio" uniqKey="Danese S" first="Silvio" last="Danese">Silvio Danese</name></country><country name="Belgique"><noRegion><name sortKey="Hindryckx, Pieter" sort="Hindryckx, Pieter" uniqKey="Hindryckx P" first="Pieter" last="Hindryckx">Pieter Hindryckx</name></noRegion></country><country name="France"><region name="Lorraine (région)"><name sortKey="Peyrin Biroulet, Laurent" sort="Peyrin Biroulet, Laurent" uniqKey="Peyrin Biroulet L" first="Laurent" last="Peyrin-Biroulet">Laurent Peyrin-Biroulet</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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