PandemieGrippaleV1, Pmc, Curation, bibRecord, 000805

Receptor for advanced glycation end products is detrimental during influenza A virus pneumonia☆

Identifieur interne : 000805 ( Pmc/Curation ); précédent : 000804; suivant : 000806

Receptor for advanced glycation end products is detrimental during influenza A virus pneumonia☆

Auteurs : Marieke A. D Van Zoelen [Pays-Bas] ; Koenraad F. Van Der Sluijs [Pays-Bas] ; Ahmed Achouiti [Pays-Bas] ; Sandrine Florquin [Pays-Bas] ; Jennie M. Braun-Pater [Pays-Bas] ; Huan Yang [États-Unis] ; Peter P. Nawroth [Allemagne] ; Kevin J. Tracey [États-Unis] ; Angelika Bierhaus [Allemagne] ; Tom Van Der Poll [Pays-Bas]

Source :

Virology [ 0042-6822 ] ; 2009.

RBID : PMC:4540231

Abstract

Pneumonia caused by influenza A virus (IAV) can have devastating effects, resulting in respiratory failure and death. The idea that a new influenza pandemic might occur in the near future has triggered renewed interests in IAV infection. The receptor for advanced glycation end products (RAGE) is expressed on different cell types and plays a key role in diverse inflammatory processes. We here investigated the role of RAGE in the host response to IAV pneumonia using wild-type (wt) and RAGE deficient (^−/−) mice. Whereas strong RAGE was constitutively expressed in the lungs of uninfected wt mice, in particular on endothelium, IAV pneumonia was associated with enhanced expression on endothelium and de novo expression on bronchial epithelium. Additionally, the high-affinity RAGE ligand high mobility group box 1 was upregulated during IAV pneumonia. RAGE^−/− mice were relatively protected from IAV induced mortality and showed an improved viral clearance and enhanced cellular T cell response and activation of neutrophils. These data suggest that RAGE is detrimental during IAV pneumonia.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4540231

DOI: 10.1016/j.virol.2009.05.032
PubMed: 19592063
PubMed Central: 4540231

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<author><name sortKey="Braun Pater, Jennie M" sort="Braun Pater, Jennie M" uniqKey="Braun Pater J" first="Jennie M." last="Braun-Pater">Jennie M. Braun-Pater</name>
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<front><div type="abstract" xml:lang="en"><p id="P1">Pneumonia caused by influenza A virus (IAV) can have devastating effects, resulting in respiratory failure and death. The idea that a new influenza pandemic might occur in the near future has triggered renewed interests in IAV infection. The receptor for advanced glycation end products (RAGE) is expressed on different cell types and plays a key role in diverse inflammatory processes. We here investigated the role of RAGE in the host response to IAV pneumonia using wild-type (<italic>wt</italic>
) and RAGE deficient (<sup>−/−</sup>
) mice. Whereas strong RAGE was constitutively expressed in the lungs of uninfected <italic>wt</italic>
 mice, in particular on endothelium, IAV pneumonia was associated with enhanced expression on endothelium and <italic>de novo</italic>
 expression on bronchial epithelium. Additionally, the high-affinity RAGE ligand high mobility group box 1 was upregulated during IAV pneumonia. RAGE<sup>−/−</sup>
 mice were relatively protected from IAV induced mortality and showed an improved viral clearance and enhanced cellular T cell response and activation of neutrophils. These data suggest that RAGE is detrimental during IAV pneumonia.</p>
</div>
</front>
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<title-group><article-title>Receptor for advanced glycation end products is detrimental during influenza A virus pneumonia<sup><xref ref-type="fn" rid="FN1">☆</xref>
</sup>
</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>van Zoelen</surname>
<given-names>Marieke A.D</given-names>
</name>
<email>M.A.vanZoelen@amc.uva.nl</email>
<xref ref-type="aff" rid="A1">a</xref>
<xref ref-type="aff" rid="A2">b</xref>
<xref ref-type="corresp" rid="cor1">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>van der Sluijs</surname>
<given-names>Koenraad F.</given-names>
</name>
<email>K.F.vandersluijs@amc.uva.nl</email>
<xref ref-type="aff" rid="A1">a</xref>
<xref ref-type="aff" rid="A3">c</xref>
<xref ref-type="aff" rid="A4">d</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Achouiti</surname>
<given-names>Ahmed</given-names>
</name>
<email>A.Achouiti@amc.uva.nl</email>
<xref ref-type="aff" rid="A1">a</xref>
<xref ref-type="aff" rid="A2">b</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Florquin</surname>
<given-names>Sandrine</given-names>
</name>
<email>S.F.Florquin@amc.uva.nl</email>
<xref ref-type="aff" rid="A5">e</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Braun-Pater</surname>
<given-names>Jennie M.</given-names>
</name>
<email>J.M.Pater@amc.amc.nl</email>
<xref ref-type="aff" rid="A1">a</xref>
<xref ref-type="aff" rid="A2">b</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Yang</surname>
<given-names>Huan</given-names>
</name>
<email>hyang@nshs.edu</email>
<xref ref-type="aff" rid="A6">f</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Nawroth</surname>
<given-names>Peter P.</given-names>
</name>
<email>Peter_Nawroth@med.uni-heidelberg.de</email>
<xref ref-type="aff" rid="A7">g</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Tracey</surname>
<given-names>Kevin J.</given-names>
</name>
<email>kjtracey@sprynet.com</email>
<xref ref-type="aff" rid="A6">f</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Bierhaus</surname>
<given-names>Angelika</given-names>
</name>
<email>angelika_bierhaus@med.uni-heidelberg.de</email>
<xref ref-type="aff" rid="A7">g</xref>
</contrib>
<contrib contrib-type="author"><name><surname>van der Poll</surname>
<given-names>Tom</given-names>
</name>
<email>T.vanderPoll@amc.uva.nl</email>
<xref ref-type="aff" rid="A1">a</xref>
<xref ref-type="aff" rid="A2">b</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>a</label>
Center for Infection and Immunity Amsterdam (CINIMA), Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands</aff>
<aff id="A2"><label>b</label>
Center for Experimental and Molecular Medicine (CEMM), Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands</aff>
<aff id="A3"><label>c</label>
Department of Pulmonology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands</aff>
<aff id="A4"><label>d</label>
Department of Experimental Immunology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands</aff>
<aff id="A5"><label>e</label>
Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands</aff>
<aff id="A6"><label>f</label>
Laboratories of Biomedical Sience, The Feinstein Institute for Medical Research, Manhassat, New York, USA</aff>
<aff id="A7"><label>g</label>
Department of Internal Medicine, University of Heidelberg, Heidelberg, Germany</aff>
<author-notes><corresp id="cor1"><label>*</label>
Corresponding author. Academic Medical Center, Room G2-130, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands. Fax: +31 206977192</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>10</day>
<month>8</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="epub"><day>09</day>
<month>7</month>
<year>2009</year>
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<pub-date pub-type="ppub"><day>1</day>
<month>9</month>
<year>2009</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>18</day>
<month>8</month>
<year>2015</year>
</pub-date>
<volume>391</volume>
<issue>2</issue>
<fpage>265</fpage>
<lpage>273</lpage>
<pmc-comment>elocation-id from pubmed: 10.1016/j.virol.2009.05.032</pmc-comment>
      <abstract><p id="P1">Pneumonia caused by influenza A virus (IAV) can have devastating effects, resulting in respiratory failure and death. The idea that a new influenza pandemic might occur in the near future has triggered renewed interests in IAV infection. The receptor for advanced glycation end products (RAGE) is expressed on different cell types and plays a key role in diverse inflammatory processes. We here investigated the role of RAGE in the host response to IAV pneumonia using wild-type (<italic>wt</italic>
) and RAGE deficient (<sup>−/−</sup>
) mice. Whereas strong RAGE was constitutively expressed in the lungs of uninfected <italic>wt</italic>
 mice, in particular on endothelium, IAV pneumonia was associated with enhanced expression on endothelium and <italic>de novo</italic>
 expression on bronchial epithelium. Additionally, the high-affinity RAGE ligand high mobility group box 1 was upregulated during IAV pneumonia. RAGE<sup>−/−</sup>
 mice were relatively protected from IAV induced mortality and showed an improved viral clearance and enhanced cellular T cell response and activation of neutrophils. These data suggest that RAGE is detrimental during IAV pneumonia.</p>
</abstract>
<kwd-group><kwd>Influenza A virus</kwd>
<kwd>Viral pneumonia</kwd>
<kwd>Receptor for advanced glycation end products</kwd>
<kwd>High mobility group box 1</kwd>
<kwd>Host defense</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>

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Receptor for advanced glycation end products is detrimental during influenza A virus pneumonia☆

Receptor for advanced glycation end products is detrimental during influenza A virus pneumonia☆

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