NF-κB as a potential therapeutic target in microbial diseases.
Identifieur interne : 000584 ( PubMed/Corpus ); précédent : 000583; suivant : 000585NF-κB as a potential therapeutic target in microbial diseases.
Auteurs : Mariateresa Vitiello ; Marilena Galdiero ; Emiliana Finamore ; Stefania Galdiero ; Massimiliano GaldieroSource :
- Molecular bioSystems [ 1742-2051 ] ; 2012.
English descriptors
- KwdEn :
- Animals, Bacterial Infections (drug therapy), Bacterial Infections (microbiology), Humans, Inflammation (microbiology), Inflammation (therapy), NF-kappa B (antagonists & inhibitors), NF-kappa B (metabolism), Signal Transduction (drug effects), Virus Diseases (drug therapy), Virus Diseases (virology).
- MESH :
- chemical , antagonists & inhibitors : NF-kappa B.
- drug effects : Signal Transduction.
- drug therapy : Bacterial Infections, Virus Diseases.
- chemical , metabolism : NF-kappa B.
- microbiology : Bacterial Infections, Inflammation.
- therapy : Inflammation.
- virology : Virus Diseases.
- Animals, Humans.
Abstract
The failure of conventional vaccines or antimicrobials to combat newly emerging pathogens such as new influenza viruses or antibiotic-resistant bacteria provides significant challenges in the identification of innovative therapeutic approaches and targets for microbial infections. Such therapies, directed towards host-cell molecules, may represent alternative options where conventional approaches face difficulties. We will largely focus on those strategies that directly target the host inflammatory response, specifically those that result in the activation of the nuclear transcription factor (NF)-κB. NF-κB plays a central role in the cellular stress response and in inflammation by controlling the expression of a network of inducers and effectors that define responses to pathogens. Therefore, the modulation of NF-κB activation and its signaling pathway offer an exceptional therapeutical strategy that could benefit from targeting a single host regulatory pathway. The use of NF-κB inhibitors or enhancers will be possible only if modulation between the host's and pathogen's advantage can be reached. Since different pathogens have developed various mechanisms to alter the activation of NF-κB, the present review will mainly focus on the role of NF-κB in microbial infections, highlighting its importance as a therapeutic target and reviewing the current understanding of how NF-κB inhibition can be considered a potential paradigm for the development of novel antimicrobial therapies.
DOI: 10.1039/c2mb05335g
PubMed: 22311336
Links to Exploration step
pubmed:22311336Le document en format XML
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Such therapies, directed towards host-cell molecules, may represent alternative options where conventional approaches face difficulties. We will largely focus on those strategies that directly target the host inflammatory response, specifically those that result in the activation of the nuclear transcription factor (NF)-κB. NF-κB plays a central role in the cellular stress response and in inflammation by controlling the expression of a network of inducers and effectors that define responses to pathogens. Therefore, the modulation of NF-κB activation and its signaling pathway offer an exceptional therapeutical strategy that could benefit from targeting a single host regulatory pathway. The use of NF-κB inhibitors or enhancers will be possible only if modulation between the host's and pathogen's advantage can be reached. Since different pathogens have developed various mechanisms to alter the activation of NF-κB, the present review will mainly focus on the role of NF-κB in microbial infections, highlighting its importance as a therapeutic target and reviewing the current understanding of how NF-κB inhibition can be considered a potential paradigm for the development of novel antimicrobial therapies.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22311336</PMID><DateCompleted><Year>2012</Year><Month>06</Month><Day>29</Day></DateCompleted><DateRevised><Year>2012</Year><Month>03</Month><Day>06</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1742-2051</ISSN><JournalIssue CitedMedium="Internet"><Volume>8</Volume><Issue>4</Issue><PubDate><Year>2012</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Molecular bioSystems</Title><ISOAbbreviation>Mol Biosyst</ISOAbbreviation></Journal><ArticleTitle>NF-κB as a potential therapeutic target in microbial diseases.</ArticleTitle><Pagination><MedlinePgn>1108-20</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1039/c2mb05335g</ELocationID><Abstract><AbstractText>The failure of conventional vaccines or antimicrobials to combat newly emerging pathogens such as new influenza viruses or antibiotic-resistant bacteria provides significant challenges in the identification of innovative therapeutic approaches and targets for microbial infections. Such therapies, directed towards host-cell molecules, may represent alternative options where conventional approaches face difficulties. We will largely focus on those strategies that directly target the host inflammatory response, specifically those that result in the activation of the nuclear transcription factor (NF)-κB. NF-κB plays a central role in the cellular stress response and in inflammation by controlling the expression of a network of inducers and effectors that define responses to pathogens. Therefore, the modulation of NF-κB activation and its signaling pathway offer an exceptional therapeutical strategy that could benefit from targeting a single host regulatory pathway. The use of NF-κB inhibitors or enhancers will be possible only if modulation between the host's and pathogen's advantage can be reached. Since different pathogens have developed various mechanisms to alter the activation of NF-κB, the present review will mainly focus on the role of NF-κB in microbial infections, highlighting its importance as a therapeutic target and reviewing the current understanding of how NF-κB inhibition can be considered a potential paradigm for the development of novel antimicrobial therapies.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Vitiello</LastName><ForeName>Mariateresa</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Experimental Medicine-II University of Naples, via De Crecchio 7, 80138, Napoli, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Galdiero</LastName><ForeName>Marilena</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Finamore</LastName><ForeName>Emiliana</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Galdiero</LastName><ForeName>Stefania</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Galdiero</LastName><ForeName>Massimiliano</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>02</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Mol Biosyst</MedlineTA><NlmUniqueID>101251620</NlmUniqueID><ISSNLinking>1742-2051</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001424" MajorTopicYN="N">Bacterial Infections</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</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="D014777" MajorTopicYN="N">Virus Diseases</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>2</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>2</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2012</Year><Month>6</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">22311336</ArticleId><ArticleId IdType="doi">10.1039/c2mb05335g</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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