The Role of Dectin-2 for Host Defense Against Disseminated Candidiasis
Identifieur interne : 000556 ( Pmc/Curation ); précédent : 000555; suivant : 000557The Role of Dectin-2 for Host Defense Against Disseminated Candidiasis
Auteurs : Daniela C. Ifrim ; Jessica Quintin ; Flavie Courjol ; Ineke Verschueren ; J. Han Van Krieken ; Frank Koentgen ; Chantal Fradin ; Neil A. R. Gow ; Leo A. B. Joosten ; Jos W. M. Van Der Meer ; Frank Van De Veerdonk ; Mihai G. NeteaSource :
- Journal of Interferon & Cytokine Research [ 1079-9907 ] ; 2016.
Abstract
Despite the fact that
Url:
DOI: 10.1089/jir.2015.0040
PubMed: 27046240
PubMed Central: 4827303
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">The Role of Dectin-2 for Host Defense Against Disseminated Candidiasis</title>
<author><name sortKey="Ifrim, Daniela C" sort="Ifrim, Daniela C" uniqKey="Ifrim D" first="Daniela C." last="Ifrim">Daniela C. Ifrim</name>
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<author><name sortKey="Quintin, Jessica" sort="Quintin, Jessica" uniqKey="Quintin J" first="Jessica" last="Quintin">Jessica Quintin</name>
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<author><name sortKey="Courjol, Flavie" sort="Courjol, Flavie" uniqKey="Courjol F" first="Flavie" last="Courjol">Flavie Courjol</name>
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<author><name sortKey="Verschueren, Ineke" sort="Verschueren, Ineke" uniqKey="Verschueren I" first="Ineke" last="Verschueren">Ineke Verschueren</name>
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<series><title level="j">Journal of Interferon & Cytokine Research</title>
<idno type="ISSN">1079-9907</idno>
<idno type="eISSN">1557-7465</idno>
<imprint><date when="2016">2016</date>
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<front><div type="abstract" xml:lang="en"><p>Despite the fact that <italic>Candida albicans</italic>
is an important human fungal pathogen and Dectin-2 is a major pattern recognition receptor for fungi, our knowledge regarding the role of Dectin-2 for the host defense against disseminated candidiasis is limited. Dectin-2 deficient (Dectin-2<sup>−/−</sup>
) mice were more susceptible to systemic candidiasis, and the susceptibility was mirrored by an elevated fungal load in the kidneys that correlated with the presence of large inflammatory foci. Phagocytosis of <italic>Candida</italic>
by the macrophages lacking the Dectin-2 receptor was moderately decreased, while production of most of the macrophage-derived cytokines from Dectin-2<sup>−/−</sup>
mice with systemic candidiasis was decreased. No striking differences among several <italic>Candida</italic>
mutants defective in mannans could be detected between naïve wild-type and Dectin-2<sup>−/−</sup>
mice, apart from the β-mannan-deficient <italic>bmt1</italic>
Δ<italic>/bmt2</italic>
Δ<italic>/bmt5</italic>
Δ triple mutant, suggesting that β-mannan may partially mask α-mannan detection, which is the major fungal structure recognized by Dectin-2. Deciphering the mechanisms responsible for host defense against the majority of <italic>C. albicans</italic>
strains represents an important step in understanding the pathophysiology of systemic candidiasis, which might lead to the development of novel immunotherapeutic strategies.</p>
</div>
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<front><journal-meta><journal-id journal-id-type="nlm-ta">J Interferon Cytokine Res</journal-id>
<journal-id journal-id-type="iso-abbrev">J. Interferon Cytokine Res</journal-id>
<journal-id journal-id-type="publisher-id">jir</journal-id>
<journal-title-group><journal-title>Journal of Interferon & Cytokine Research</journal-title>
</journal-title-group>
<issn pub-type="ppub">1079-9907</issn>
<issn pub-type="epub">1557-7465</issn>
<publisher><publisher-name>Mary Ann Liebert, Inc.</publisher-name>
<publisher-loc>140 Huguenot Street, 3rd FloorNew Rochelle, NY 10801USA</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">27046240</article-id>
<article-id pub-id-type="pmc">4827303</article-id>
<article-id pub-id-type="publisher-id">10.1089/jir.2015.0040</article-id>
<article-id pub-id-type="doi">10.1089/jir.2015.0040</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Research Reports</subject>
</subj-group>
</article-categories>
<title-group><article-title>The Role of Dectin-2 for Host Defense Against Disseminated Candidiasis</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Ifrim</surname>
<given-names>Daniela C.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Quintin</surname>
<given-names>Jessica</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Courjol</surname>
<given-names>Flavie</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>2,</sup>
</xref>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Verschueren</surname>
<given-names>Ineke</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>van Krieken</surname>
<given-names>J. Han</given-names>
</name>
<xref ref-type="aff" rid="aff4"><sup>4</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Koentgen</surname>
<given-names>Frank</given-names>
</name>
<xref ref-type="aff" rid="aff5"><sup>5</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Fradin</surname>
<given-names>Chantal</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>2,</sup>
</xref>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Gow</surname>
<given-names>Neil A.R.</given-names>
</name>
<xref ref-type="aff" rid="aff6"><sup>6</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Joosten</surname>
<given-names>Leo A.B.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>van der Meer</surname>
<given-names>Jos W.M.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>van de Veerdonk</surname>
<given-names>Frank</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author" corresp="yes"><name><surname>Netea</surname>
<given-names>Mihai G.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<aff id="aff1"><label><sup>1</sup>
</label>
Department of Internal Medicine, Radboud Center for Infectious Diseases (RCI),<institution>Radboud University Nijmegen Medical Centre</institution>
, Nijmegen,<country>The Netherlands</country>
.</aff>
<aff id="aff2"><label><sup>2</sup>
</label>
<institution>Inserm U995</institution>
, Lille,<country>France</country>
.</aff>
<aff id="aff3"><label><sup>3</sup>
</label>
<institution>Université de Lille</institution>
, Faculté de Médecine, Lille,<country>France</country>
.</aff>
<aff id="aff4"><label><sup>4</sup>
</label>
Department of Pathology,<institution>Radboud University Nijmegen Medical Centre</institution>
, Nijmegen,<country>The Netherlands</country>
.</aff>
<aff id="aff5"><label><sup>5</sup>
</label>
<institution>Ozgene Pty Ltd</institution>
, Bentley DC,<country>Australia</country>
.</aff>
<aff id="aff6"><label><sup>6</sup>
</label>
Aberdeen Fungal Group, School of Medical Sciences, Institute of Medical Sciences,<institution>University of Aberdeen</institution>
, Aberdeen,<country>United Kingdom</country>
.</aff>
</contrib-group>
<author-notes><corresp><addr-line>Address correspondence to:</addr-line>
<addr-line><italic>Dr. Mihai G. Netea</italic>
</addr-line>
<addr-line><italic>Department of Internal Medicine (463)</italic>
</addr-line>
<addr-line><italic>Radboud Center for Infectious Diseases (RCI)</italic>
</addr-line>
<institution><italic>Radboud University Nijmegen Medical Centre</italic>
</institution>
<addr-line><italic>Geert Grooteplein Zuid 8</italic>
</addr-line>
<addr-line><italic>Nijmegen 6525 GA</italic>
</addr-line>
<country>The Netherlands</country>
<break></break>
<italic>E-mail:</italic>
<email xlink:href="mailto:mihai.netea@radboudumc.nl">mihai.netea@radboudumc.nl</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub"><day>01</day>
<month>4</month>
<year>2016</year>
<pmc-comment>string-date: April 2016</pmc-comment>
</pub-date>
<pub-date pub-type="pmc-release"><day>01</day>
<month>4</month>
<year>2016</year>
<pmc-comment>string-date: April 2016</pmc-comment>
</pub-date>
<pmc-comment> PMC Release delay is 0 months and 0 days and was based on the
. </pmc-comment>
<volume>36</volume>
<issue>4</issue>
<fpage>267</fpage>
<lpage>276</lpage>
<history><date date-type="received"><day>08</day>
<month>4</month>
<year>2015</year>
<pmc-comment>string-date: Received 8 April 2015</pmc-comment>
</date>
<date date-type="accepted"><day>06</day>
<month>11</month>
<year>2015</year>
<pmc-comment>string-date: Accepted 6 November 2015</pmc-comment>
</date>
</history>
<permissions><copyright-statement>© Daniela C. Ifrim et al. 2016; Published by Mary Ann Liebert, Inc.</copyright-statement>
<copyright-year>2016</copyright-year>
<license license-type="open-access"><license-p>This Open Access article is distributed under the terms of the Creative Commons License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0">http://creativecommons.org/licenses/by/4.0</ext-link>
), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited.</license-p>
</license>
</permissions>
<self-uri content-type="pdf" xlink:type="simple" xlink:href="jir.2015.0040.pdf"></self-uri>
<abstract><p>Despite the fact that <italic>Candida albicans</italic>
is an important human fungal pathogen and Dectin-2 is a major pattern recognition receptor for fungi, our knowledge regarding the role of Dectin-2 for the host defense against disseminated candidiasis is limited. Dectin-2 deficient (Dectin-2<sup>−/−</sup>
) mice were more susceptible to systemic candidiasis, and the susceptibility was mirrored by an elevated fungal load in the kidneys that correlated with the presence of large inflammatory foci. Phagocytosis of <italic>Candida</italic>
by the macrophages lacking the Dectin-2 receptor was moderately decreased, while production of most of the macrophage-derived cytokines from Dectin-2<sup>−/−</sup>
mice with systemic candidiasis was decreased. No striking differences among several <italic>Candida</italic>
mutants defective in mannans could be detected between naïve wild-type and Dectin-2<sup>−/−</sup>
mice, apart from the β-mannan-deficient <italic>bmt1</italic>
Δ<italic>/bmt2</italic>
Δ<italic>/bmt5</italic>
Δ triple mutant, suggesting that β-mannan may partially mask α-mannan detection, which is the major fungal structure recognized by Dectin-2. Deciphering the mechanisms responsible for host defense against the majority of <italic>C. albicans</italic>
strains represents an important step in understanding the pathophysiology of systemic candidiasis, which might lead to the development of novel immunotherapeutic strategies.</p>
</abstract>
<counts><fig-count count="6"></fig-count>
<ref-count count="37"></ref-count>
<page-count count="10"></page-count>
</counts>
</article-meta>
</front>
</pmc>
</record>
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