Histoplasma Responses to Nutritional Immunity Imposed by Macrophage Activation
Identifieur interne : 000A86 ( Pmc/Checkpoint ); précédent : 000A85; suivant : 000A87Histoplasma Responses to Nutritional Immunity Imposed by Macrophage Activation
Auteurs : Peter J. Brechting ; Chad A. RappleyeSource :
- Journal of Fungi [ 2309-608X ] ; 2019.
Abstract
The fungal pathogen
Url:
DOI: 10.3390/jof5020045
PubMed: 31195617
PubMed Central: 6616858
Affiliations:
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PMC:6616858Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en"><italic>Histoplasma</italic>
Responses to Nutritional Immunity Imposed by Macrophage Activation</title>
<author><name sortKey="Brechting, Peter J" sort="Brechting, Peter J" uniqKey="Brechting P" first="Peter J." last="Brechting">Peter J. Brechting</name>
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<author><name sortKey="Rappleye, Chad A" sort="Rappleye, Chad A" uniqKey="Rappleye C" first="Chad A." last="Rappleye">Chad A. Rappleye</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main"><italic>Histoplasma</italic>
Responses to Nutritional Immunity Imposed by Macrophage Activation</title>
<author><name sortKey="Brechting, Peter J" sort="Brechting, Peter J" uniqKey="Brechting P" first="Peter J." last="Brechting">Peter J. Brechting</name>
</author>
<author><name sortKey="Rappleye, Chad A" sort="Rappleye, Chad A" uniqKey="Rappleye C" first="Chad A." last="Rappleye">Chad A. Rappleye</name>
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<series><title level="j">Journal of Fungi</title>
<idno type="eISSN">2309-608X</idno>
<imprint><date when="2019">2019</date>
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<front><div type="abstract" xml:lang="en"><p>The fungal pathogen <italic>Histoplasma capsulatum</italic>
resides within the phagosome of host phagocytic cells. Within this intracellular compartment, <italic>Histoplasma</italic>
yeast replication requires the acquisition of several essential nutrients, including metal ions. Recent work has shown that while iron, zinc, and copper are sufficiently abundant in resting macrophages, cytokine activation of these host cells causes restriction of these metals from intracellular yeasts as a form of nutritional immunity. Faced with limited iron availability in the phagosome following macrophage activation by IFN-γ, <italic>Histoplasma</italic>
yeasts secrete iron-scavenging siderophores and employ multiple strategies for reduction of ferric iron to the more physiologically useful ferrous form. IFN-γ activation of macrophages also limits availability of copper in the phagosome, forcing <italic>Histoplasma</italic>
reliance on the high affinity Ctr3 copper importer for copper acquisition. GM-CSF activation stimulates macrophage production of zinc-chelating metallothioneins and zinc transporters to sequester zinc from <italic>Histoplasma</italic>
yeasts. In response, <italic>Histoplasma</italic>
yeasts express the Zrt2 zinc importer. These findings highlight the dynamics of phagosomal metal ion concentrations in host-pathogen interactions and explain one mechanism by which macrophages become a less permissive environment for <italic>Histoplasma</italic>
replication with the onset of adaptive immunity.</p>
</div>
</front>
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</TEI>
<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Fungi (Basel)</journal-id>
<journal-id journal-id-type="iso-abbrev">J Fungi (Basel)</journal-id>
<journal-id journal-id-type="publisher-id">jof</journal-id>
<journal-title-group><journal-title>Journal of Fungi</journal-title>
</journal-title-group>
<issn pub-type="epub">2309-608X</issn>
<publisher><publisher-name>MDPI</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">31195617</article-id>
<article-id pub-id-type="pmc">6616858</article-id>
<article-id pub-id-type="doi">10.3390/jof5020045</article-id>
<article-id pub-id-type="publisher-id">jof-05-00045</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review</subject>
</subj-group>
</article-categories>
<title-group><article-title><italic>Histoplasma</italic>
Responses to Nutritional Immunity Imposed by Macrophage Activation</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Brechting</surname>
<given-names>Peter J.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0001-7880-5958</contrib-id>
<name><surname>Rappleye</surname>
<given-names>Chad A.</given-names>
</name>
<xref rid="c1-jof-05-00045" ref-type="corresp">*</xref>
</contrib>
</contrib-group>
<aff id="af1-jof-05-00045">Department of Microbiology, Ohio State University, Columbus, OH 43210, USA;<email>brechting.1@osu.edu</email>
</aff>
<author-notes><corresp id="c1-jof-05-00045"><label>*</label>
Correspondence: <email>rappleye.1@osu.edu</email>
; Tel.: +1-614-247-2718</corresp>
</author-notes>
<pub-date pub-type="epub"><day>05</day>
<month>6</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="collection"><month>6</month>
<year>2019</year>
</pub-date>
<volume>5</volume>
<issue>2</issue>
<elocation-id>45</elocation-id>
<history><date date-type="received"><day>13</day>
<month>5</month>
<year>2019</year>
</date>
<date date-type="accepted"><day>31</day>
<month>5</month>
<year>2019</year>
</date>
</history>
<permissions><copyright-statement>© 2019 by the authors.</copyright-statement>
<copyright-year>2019</copyright-year>
<license license-type="open-access"><license-p>Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) 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>
).</license-p>
</license>
</permissions>
<abstract><p>The fungal pathogen <italic>Histoplasma capsulatum</italic>
resides within the phagosome of host phagocytic cells. Within this intracellular compartment, <italic>Histoplasma</italic>
yeast replication requires the acquisition of several essential nutrients, including metal ions. Recent work has shown that while iron, zinc, and copper are sufficiently abundant in resting macrophages, cytokine activation of these host cells causes restriction of these metals from intracellular yeasts as a form of nutritional immunity. Faced with limited iron availability in the phagosome following macrophage activation by IFN-γ, <italic>Histoplasma</italic>
yeasts secrete iron-scavenging siderophores and employ multiple strategies for reduction of ferric iron to the more physiologically useful ferrous form. IFN-γ activation of macrophages also limits availability of copper in the phagosome, forcing <italic>Histoplasma</italic>
reliance on the high affinity Ctr3 copper importer for copper acquisition. GM-CSF activation stimulates macrophage production of zinc-chelating metallothioneins and zinc transporters to sequester zinc from <italic>Histoplasma</italic>
yeasts. In response, <italic>Histoplasma</italic>
yeasts express the Zrt2 zinc importer. These findings highlight the dynamics of phagosomal metal ion concentrations in host-pathogen interactions and explain one mechanism by which macrophages become a less permissive environment for <italic>Histoplasma</italic>
replication with the onset of adaptive immunity.</p>
</abstract>
<kwd-group><kwd><italic>Histoplasma</italic>
</kwd>
<kwd>macrophage</kwd>
<kwd>virulence</kwd>
<kwd>phagosome</kwd>
<kwd>iron</kwd>
<kwd>zinc</kwd>
<kwd>copper</kwd>
<kwd>immunity</kwd>
</kwd-group>
</article-meta>
</front>
<floats-group><fig id="jof-05-00045-f001" orientation="portrait" position="float"><label>Figure 1</label>
<caption><p>Metal acquisition mechanisms of intraphagosomal <italic>Histoplasma</italic>
combat metal sequestration by infected macrophages triggered by inflammatory cytokines. In resting macrophages (left panel) iron, zinc, and copper levels are sufficient for <italic>Histoplasma</italic>
growth. Upon activation (right panel), infected macrophages attempt to deprive <italic>Histoplasma</italic>
of essential metals through divalent cation exporters (e.g., Nramp1 and Slc30a7), zinc chelating metallothioneins, and as-yet undefined mechanisms. Under these metal-limited conditions, <italic>Histoplasma</italic>
in turn upregulates the copper and zinc importers, Ctr3 and Zrt2, respectively. Additionally, <italic>Histoplasma</italic>
secretes siderophores to scavenge iron, as well as the Ggt1 protein, which catalyzes a ferric reduction pathway, providing ferrous iron for the yeast.</p>
</caption>
<graphic xlink:href="jof-05-00045-g001"></graphic>
</fig>
</floats-group>
</pmc>
<affiliations><list></list>
<tree><noCountry><name sortKey="Brechting, Peter J" sort="Brechting, Peter J" uniqKey="Brechting P" first="Peter J." last="Brechting">Peter J. Brechting</name>
<name sortKey="Rappleye, Chad A" sort="Rappleye, Chad A" uniqKey="Rappleye C" first="Chad A." last="Rappleye">Chad A. Rappleye</name>
</noCountry>
</tree>
</affiliations>
</record>
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