AustralieFrV1, Main, Exploration, bibRecord, 006C22

Critical Role of cRel Subunit of NF-KB in Sepsis Survival

Identifieur interne : 006C22 ( Main/Exploration ); précédent : 006C21; suivant : 006C23

Critical Role of cRel Subunit of NF-KB in Sepsis Survival

Auteurs : Emilie Courtine [France] ; Frederic Pene [France] ; Nicolas Cagnard [France] ; Julie Toubiana [France] ; Catherine Fitting [France] ; Jessy Brocheton [France] ; Christophe Rousseau [France] ; Steve Gerondakis [Australie] ; Jean-Daniel Chiche [France] ; Fatah Ouaaz [France] ; Jean-Paul Mira [France]

Source :

Infection and immunity [ 0019-9567 ] ; 2011.

RBID : Pascal:11-0240874

Descripteurs français

Pascal (Inist)
- Sousunité, Facteur transcription NFκB, Immunité, Syndrome septique.

English descriptors

KwdEn :
- Immunity, Sepsis syndrome, Subunit, Transcription factor NFκB.

Abstract

NF-κB is a critical regulator of gene expression during severe infections. NF-κB comprises homo- and heterodimers of proteins from the Rel family. Among them, p50 and p65 have been clearly implicated in the pathophysiology of sepsis. In contrast, the role of cRel in sepsis is still controversial and has been poorly studied in single-pathogen infections. We aimed to investigate the consequences of cRel deficiency in a cecal ligation and puncture (CLP) model of sepsis. We have approached the underlying mechanisms of host defense by analyzing bacterial clearance, systemic inflammation, and the distribution of spleen dendritic cell subsets. Moreover, by using a genome-wide technology, we have also analyzed the CLP-induced modifications in gene expression profiles both in wild-type (wt) and in rel^-/- mice. The absence of cRel enhances mortality due to polymicrobial sepsis. Despite normal pathogen clearance, cRel deficiency leads to an altered systemic inflammatory response associated with a sustained loss of the spleen lymphoid dendritic cells. Furthermore, a whole-blood microarray study reveals that the differential outcome between wt and rel^-/- mice during sepsis is preceded by remarkable changes in the expression of hundreds of genes involved in aspects of host-pathogen interaction, such as host survival and lipid metabolism. In conclusion, cRel is a key NF-κB member required for host antimicrobial defenses and a regulatory transcription subunit that controls the inflammatory and immune responses in severe infection.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3088128

Affiliations:

Le document en format XML

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</analytic>
<series><title level="j" type="main">Infection and immunity</title>
<title level="j" type="abbreviated">Infect. immun.</title>
<idno type="ISSN">0019-9567</idno>
<imprint><date when="2011">2011</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Infection and immunity</title>
<title level="j" type="abbreviated">Infect. immun.</title>
<idno type="ISSN">0019-9567</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Immunity</term>
<term>Sepsis syndrome</term>
<term>Subunit</term>
<term>Transcription factor NFκB</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Sousunité</term>
<term>Facteur transcription NFκB</term>
<term>Immunité</term>
<term>Syndrome septique</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">NF-κB is a critical regulator of gene expression during severe infections. NF-κB comprises homo- and heterodimers of proteins from the Rel family. Among them, p50 and p65 have been clearly implicated in the pathophysiology of sepsis. In contrast, the role of cRel in sepsis is still controversial and has been poorly studied in single-pathogen infections. We aimed to investigate the consequences of cRel deficiency in a cecal ligation and puncture (CLP) model of sepsis. We have approached the underlying mechanisms of host defense by analyzing bacterial clearance, systemic inflammation, and the distribution of spleen dendritic cell subsets. Moreover, by using a genome-wide technology, we have also analyzed the CLP-induced modifications in gene expression profiles both in wild-type (wt) and in rel<sup>-/-</sup>
 mice. The absence of cRel enhances mortality due to polymicrobial sepsis. Despite normal pathogen clearance, cRel deficiency leads to an altered systemic inflammatory response associated with a sustained loss of the spleen lymphoid dendritic cells. Furthermore, a whole-blood microarray study reveals that the differential outcome between wt and rel<sup>-/-</sup>
 mice during sepsis is preceded by remarkable changes in the expression of hundreds of genes involved in aspects of host-pathogen interaction, such as host survival and lipid metabolism. In conclusion, cRel is a key NF-κB member required for host antimicrobial defenses and a regulatory transcription subunit that controls the inflammatory and immune responses in severe infection.</div>
</front>
</TEI>
<affiliations><list><country><li>Australie</li>
<li>France</li>
</country>
<region><li>Île-de-France</li>
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</settlement>
<orgName><li>Université Paris-Descartes</li>
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<tree><country name="France"><region name="Île-de-France"><name sortKey="Courtine, Emilie" sort="Courtine, Emilie" uniqKey="Courtine E" first="Emilie" last="Courtine">Emilie Courtine</name>
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<name sortKey="Brocheton, Jessy" sort="Brocheton, Jessy" uniqKey="Brocheton J" first="Jessy" last="Brocheton">Jessy Brocheton</name>
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<name sortKey="Chiche, Jean Daniel" sort="Chiche, Jean Daniel" uniqKey="Chiche J" first="Jean-Daniel" last="Chiche">Jean-Daniel Chiche</name>
<name sortKey="Chiche, Jean Daniel" sort="Chiche, Jean Daniel" uniqKey="Chiche J" first="Jean-Daniel" last="Chiche">Jean-Daniel Chiche</name>
<name sortKey="Chiche, Jean Daniel" sort="Chiche, Jean Daniel" uniqKey="Chiche J" first="Jean-Daniel" last="Chiche">Jean-Daniel Chiche</name>
<name sortKey="Courtine, Emilie" sort="Courtine, Emilie" uniqKey="Courtine E" first="Emilie" last="Courtine">Emilie Courtine</name>
<name sortKey="Fitting, Catherine" sort="Fitting, Catherine" uniqKey="Fitting C" first="Catherine" last="Fitting">Catherine Fitting</name>
<name sortKey="Mira, Jean Paul" sort="Mira, Jean Paul" uniqKey="Mira J" first="Jean-Paul" last="Mira">Jean-Paul Mira</name>
<name sortKey="Mira, Jean Paul" sort="Mira, Jean Paul" uniqKey="Mira J" first="Jean-Paul" last="Mira">Jean-Paul Mira</name>
<name sortKey="Mira, Jean Paul" sort="Mira, Jean Paul" uniqKey="Mira J" first="Jean-Paul" last="Mira">Jean-Paul Mira</name>
<name sortKey="Ouaaz, Fatah" sort="Ouaaz, Fatah" uniqKey="Ouaaz F" first="Fatah" last="Ouaaz">Fatah Ouaaz</name>
<name sortKey="Ouaaz, Fatah" sort="Ouaaz, Fatah" uniqKey="Ouaaz F" first="Fatah" last="Ouaaz">Fatah Ouaaz</name>
<name sortKey="Pene, Frederic" sort="Pene, Frederic" uniqKey="Pene F" first="Frederic" last="Pene">Frederic Pene</name>
<name sortKey="Pene, Frederic" sort="Pene, Frederic" uniqKey="Pene F" first="Frederic" last="Pene">Frederic Pene</name>
<name sortKey="Pene, Frederic" sort="Pene, Frederic" uniqKey="Pene F" first="Frederic" last="Pene">Frederic Pene</name>
<name sortKey="Rousseau, Christophe" sort="Rousseau, Christophe" uniqKey="Rousseau C" first="Christophe" last="Rousseau">Christophe Rousseau</name>
<name sortKey="Rousseau, Christophe" sort="Rousseau, Christophe" uniqKey="Rousseau C" first="Christophe" last="Rousseau">Christophe Rousseau</name>
<name sortKey="Toubiana, Julie" sort="Toubiana, Julie" uniqKey="Toubiana J" first="Julie" last="Toubiana">Julie Toubiana</name>
<name sortKey="Toubiana, Julie" sort="Toubiana, Julie" uniqKey="Toubiana J" first="Julie" last="Toubiana">Julie Toubiana</name>
</country>
<country name="Australie"><noRegion><name sortKey="Gerondakis, Steve" sort="Gerondakis, Steve" uniqKey="Gerondakis S" first="Steve" last="Gerondakis">Steve Gerondakis</name>
</noRegion>
<name sortKey="Gerondakis, Steve" sort="Gerondakis, Steve" uniqKey="Gerondakis S" first="Steve" last="Gerondakis">Steve Gerondakis</name>
<name sortKey="Gerondakis, Steve" sort="Gerondakis, Steve" uniqKey="Gerondakis S" first="Steve" last="Gerondakis">Steve Gerondakis</name>
</country>
</tree>
</affiliations>
</record>

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Critical Role of cRel Subunit of NF-KB in Sepsis Survival

Critical Role of cRel Subunit of NF-KB in Sepsis Survival

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