Malaria infection promotes a selective expression of kinin receptors in murine liver
Identifieur interne : 000608 ( Pmc/Checkpoint ); précédent : 000607; suivant : 000609Malaria infection promotes a selective expression of kinin receptors in murine liver
Auteurs : Priscilla D. S. Ventura [Brésil] ; Carolina P. F. Carvalho [Brésil] ; Nilana M. T. Barros [Brésil] ; Leonardo Martins-Silva [Brésil] ; Edilson O. Dantas [Brésil] ; Carolina Martinez [Brésil] ; Pollyana M. S. Melo [Brésil] ; João B. Pesquero [Brésil] ; Adriana K. Carmona [Brésil] ; Marcia R. Nagaoka [Brésil] ; Marcos L. Gazarini [Brésil]Source :
- Malaria Journal [ 1475-2875 ] ; 2019.
Abstract
Malaria represents a worldwide medical emergency affecting mainly poor areas.
Balb/C mice infected by
It was verified that captopril treatment caused host death during the peak of malaria infection (parasitaemia about 45%). B1R expression was stimulated in endothelial cells of sinusoids and other blood vessels of mice liver infected by
Thus, it was observed through in vivo studies that the vasodilation induced by plasma ACE inhibition increases mice mortality during
Url:
DOI: 10.1186/s12936-019-2846-3
PubMed: 31234939
PubMed Central: 6591901
Affiliations:
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<author><name sortKey="Melo, Pollyana M S" sort="Melo, Pollyana M S" uniqKey="Melo P" first="Pollyana M. S." last="Melo">Pollyana M. S. Melo</name>
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<author><name sortKey="Pesquero, Joao B" sort="Pesquero, Joao B" uniqKey="Pesquero J" first="João B." last="Pesquero">João B. Pesquero</name>
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São Paulo, Brazil</nlm:aff>
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<author><name sortKey="Carmona, Adriana K" sort="Carmona, Adriana K" uniqKey="Carmona A" first="Adriana K." last="Carmona">Adriana K. Carmona</name>
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São Paulo, Brazil</nlm:aff>
<country xml:lang="fr">Brésil</country>
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<author><name sortKey="Nagaoka, Marcia R" sort="Nagaoka, Marcia R" uniqKey="Nagaoka M" first="Marcia R." last="Nagaoka">Marcia R. Nagaoka</name>
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<author><name sortKey="Gazarini, Marcos L" sort="Gazarini, Marcos L" uniqKey="Gazarini M" first="Marcos L." last="Gazarini">Marcos L. Gazarini</name>
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<series><title level="j">Malaria Journal</title>
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<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p id="Par1">Malaria represents a worldwide medical emergency affecting mainly poor areas. <italic>Plasmodium</italic>
parasites during blood stages can release kinins to the extracellular space after internalization of host kininogen inside erythrocytes and these released peptides could represent an important mechanism in liver pathophysiology by activation of calcium signaling pathway in endothelial cells of vertebrate host. Receptors (B1 and B2) activated by kinins peptides are important elements for the control of haemodynamics in liver and its physiology. The aim of this study was to identify changes in the liver host responses (i.e. kinin receptors expression and localization) and the effect of ACE inhibition during malaria infection using a murine model.</p>
</sec>
<sec><title>Methods</title>
<p id="Par2">Balb/C mice infected by <italic>Plasmodium chabaudi</italic>
were treated with captopril, an angiotensin I-converting enzyme (ACE) inhibitor, used alone or in association with the anti-malarial chloroquine in order to study the effect of ACE inhibition on mice survival and the activation of liver responses involving B1R and B2R signaling pathways. The kinin receptors (B1R and B2R) expression and localization was analysed in liver by western blotting and immunolocalization in different conditions.</p>
</sec>
<sec><title>Results</title>
<p id="Par3">It was verified that captopril treatment caused host death during the peak of malaria infection (parasitaemia about 45%). B1R expression was stimulated in endothelial cells of sinusoids and other blood vessels of mice liver infected by <italic>P. chabaudi</italic>
. At the same time, it was also demonstrated that B1R knockout mice infected presented a significant reduction of survival. However, the infection did not alter the B2R levels and localization in liver blood vessels.</p>
</sec>
<sec><title>Conclusions</title>
<p id="Par4">Thus, it was observed through in vivo studies that the vasodilation induced by plasma ACE inhibition increases mice mortality during <italic>P. chabaudi</italic>
infection. Besides, it was also seen that the anti-malarial chloroquine causes changes in B1R expression in liver, even after days of parasite clearance. The differential expression of B1R and B2R in liver during malaria infection may have an important role in the disease pathophysiology and represents an issue for clinical treatments.</p>
</sec>
</div>
</front>
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<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Malar J</journal-id>
<journal-id journal-id-type="iso-abbrev">Malar. J</journal-id>
<journal-title-group><journal-title>Malaria Journal</journal-title>
</journal-title-group>
<issn pub-type="epub">1475-2875</issn>
<publisher><publisher-name>BioMed Central</publisher-name>
<publisher-loc>London</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">31234939</article-id>
<article-id pub-id-type="pmc">6591901</article-id>
<article-id pub-id-type="publisher-id">2846</article-id>
<article-id pub-id-type="doi">10.1186/s12936-019-2846-3</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Research</subject>
</subj-group>
</article-categories>
<title-group><article-title>Malaria infection promotes a selective expression of kinin receptors in murine liver</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Ventura</surname>
<given-names>Priscilla D. S.</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Carvalho</surname>
<given-names>Carolina P. F.</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Barros</surname>
<given-names>Nilana M. T.</given-names>
</name>
<xref ref-type="aff" rid="Aff2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Martins-Silva</surname>
<given-names>Leonardo</given-names>
</name>
<xref ref-type="aff" rid="Aff4">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Dantas</surname>
<given-names>Edilson O.</given-names>
</name>
<xref ref-type="aff" rid="Aff3">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Martinez</surname>
<given-names>Carolina</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Melo</surname>
<given-names>Pollyana M. S.</given-names>
</name>
<xref ref-type="aff" rid="Aff4">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Pesquero</surname>
<given-names>João B.</given-names>
</name>
<xref ref-type="aff" rid="Aff4">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Carmona</surname>
<given-names>Adriana K.</given-names>
</name>
<xref ref-type="aff" rid="Aff4">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Nagaoka</surname>
<given-names>Marcia R.</given-names>
</name>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">http://orcid.org/0000-0002-3882-6831</contrib-id>
<name><surname>Gazarini</surname>
<given-names>Marcos L.</given-names>
</name>
<address><email>marcos.gazarini@unifesp.br</email>
</address>
<xref ref-type="aff" rid="Aff1">1</xref>
</contrib>
<aff id="Aff1"><label>1</label>
<institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0514 7202</institution-id>
<institution-id institution-id-type="GRID">grid.411249.b</institution-id>
<institution>Departamento de Biociências,</institution>
<institution>Universidade Federal de São Paulo,</institution>
</institution-wrap>
Rua Silva Jardim 136, Lab 329, 3ºandar, Vila Mathias, Santos, 11015020 Brazil</aff>
<aff id="Aff2"><label>2</label>
<institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0514 7202</institution-id>
<institution-id institution-id-type="GRID">grid.411249.b</institution-id>
<institution>Departamento de Ciências Biológicas,</institution>
<institution>Universidade Federal de São Paulo,</institution>
</institution-wrap>
Diadema, Brazil</aff>
<aff id="Aff3"><label>3</label>
<institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0514 7202</institution-id>
<institution-id institution-id-type="GRID">grid.411249.b</institution-id>
<institution>Departamento de Medicina,</institution>
<institution>Universidade Federal de São Paulo,</institution>
</institution-wrap>
São Paulo, Brazil</aff>
<aff id="Aff4"><label>4</label>
<institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0514 7202</institution-id>
<institution-id institution-id-type="GRID">grid.411249.b</institution-id>
<institution>Departamento de Biofísica,</institution>
<institution>Universidade Federal de São Paulo,</institution>
</institution-wrap>
São Paulo, Brazil</aff>
</contrib-group>
<pub-date pub-type="epub"><day>24</day>
<month>6</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>24</day>
<month>6</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="collection"><year>2019</year>
</pub-date>
<volume>18</volume>
<elocation-id>213</elocation-id>
<history><date date-type="received"><day>21</day>
<month>2</month>
<year>2019</year>
</date>
<date date-type="accepted"><day>18</day>
<month>6</month>
<year>2019</year>
</date>
</history>
<permissions><copyright-statement>© The Author(s) 2019</copyright-statement>
<license license-type="OpenAccess"><license-p><bold>Open Access</bold>
This article is distributed under the terms of the Creative Commons Attribution 4.0 International 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 you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/publicdomain/zero/1.0/">http://creativecommons.org/publicdomain/zero/1.0/</ext-link>
) applies to the data made available in this article, unless otherwise stated.</license-p>
</license>
</permissions>
<abstract id="Abs1"><sec><title>Background</title>
<p id="Par1">Malaria represents a worldwide medical emergency affecting mainly poor areas. <italic>Plasmodium</italic>
parasites during blood stages can release kinins to the extracellular space after internalization of host kininogen inside erythrocytes and these released peptides could represent an important mechanism in liver pathophysiology by activation of calcium signaling pathway in endothelial cells of vertebrate host. Receptors (B1 and B2) activated by kinins peptides are important elements for the control of haemodynamics in liver and its physiology. The aim of this study was to identify changes in the liver host responses (i.e. kinin receptors expression and localization) and the effect of ACE inhibition during malaria infection using a murine model.</p>
</sec>
<sec><title>Methods</title>
<p id="Par2">Balb/C mice infected by <italic>Plasmodium chabaudi</italic>
were treated with captopril, an angiotensin I-converting enzyme (ACE) inhibitor, used alone or in association with the anti-malarial chloroquine in order to study the effect of ACE inhibition on mice survival and the activation of liver responses involving B1R and B2R signaling pathways. The kinin receptors (B1R and B2R) expression and localization was analysed in liver by western blotting and immunolocalization in different conditions.</p>
</sec>
<sec><title>Results</title>
<p id="Par3">It was verified that captopril treatment caused host death during the peak of malaria infection (parasitaemia about 45%). B1R expression was stimulated in endothelial cells of sinusoids and other blood vessels of mice liver infected by <italic>P. chabaudi</italic>
. At the same time, it was also demonstrated that B1R knockout mice infected presented a significant reduction of survival. However, the infection did not alter the B2R levels and localization in liver blood vessels.</p>
</sec>
<sec><title>Conclusions</title>
<p id="Par4">Thus, it was observed through in vivo studies that the vasodilation induced by plasma ACE inhibition increases mice mortality during <italic>P. chabaudi</italic>
infection. Besides, it was also seen that the anti-malarial chloroquine causes changes in B1R expression in liver, even after days of parasite clearance. The differential expression of B1R and B2R in liver during malaria infection may have an important role in the disease pathophysiology and represents an issue for clinical treatments.</p>
</sec>
</abstract>
<kwd-group xml:lang="en"><title>Keywords</title>
<kwd><italic>Plasmodium</italic>
</kwd>
<kwd>Malaria</kwd>
<kwd>Kinin receptors</kwd>
<kwd>Liver</kwd>
<kwd>Captopril</kwd>
</kwd-group>
<funding-group><award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">http://dx.doi.org/10.13039/501100001807</institution-id>
<institution>Fundação de Amparo à Pesquisa do Estado de São Paulo</institution>
</institution-wrap>
</funding-source>
<award-id>09/54598-9</award-id>
<award-id>19/13601-9</award-id>
<award-id>08/55928-0</award-id>
<award-id>14/22206-2</award-id>
<award-id>15/11861-2</award-id>
<principal-award-recipient><name><surname>Carvalho</surname>
<given-names>Carolina P. F.</given-names>
</name>
<name><surname>Carmona</surname>
<given-names>Adriana K.</given-names>
</name>
<name><surname>Nagaoka</surname>
<given-names>Marcia R.</given-names>
</name>
<name><surname>Gazarini</surname>
<given-names>Marcos L.</given-names>
</name>
</principal-award-recipient>
</award-group>
</funding-group>
<funding-group><award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">http://dx.doi.org/10.13039/501100003593</institution-id>
<institution>Conselho Nacional de Desenvolvimento Científico e Tecnológico</institution>
</institution-wrap>
</funding-source>
<award-id>fellowship</award-id>
</award-group>
</funding-group>
<custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name>
<meta-value>© The Author(s) 2019</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>Brésil</li>
</country>
</list>
<tree><country name="Brésil"><noRegion><name sortKey="Ventura, Priscilla D S" sort="Ventura, Priscilla D S" uniqKey="Ventura P" first="Priscilla D. S." last="Ventura">Priscilla D. S. Ventura</name>
</noRegion>
<name sortKey="Barros, Nilana M T" sort="Barros, Nilana M T" uniqKey="Barros N" first="Nilana M. T." last="Barros">Nilana M. T. Barros</name>
<name sortKey="Carmona, Adriana K" sort="Carmona, Adriana K" uniqKey="Carmona A" first="Adriana K." last="Carmona">Adriana K. Carmona</name>
<name sortKey="Carvalho, Carolina P F" sort="Carvalho, Carolina P F" uniqKey="Carvalho C" first="Carolina P. F." last="Carvalho">Carolina P. F. Carvalho</name>
<name sortKey="Dantas, Edilson O" sort="Dantas, Edilson O" uniqKey="Dantas E" first="Edilson O." last="Dantas">Edilson O. Dantas</name>
<name sortKey="Gazarini, Marcos L" sort="Gazarini, Marcos L" uniqKey="Gazarini M" first="Marcos L." last="Gazarini">Marcos L. Gazarini</name>
<name sortKey="Martinez, Carolina" sort="Martinez, Carolina" uniqKey="Martinez C" first="Carolina" last="Martinez">Carolina Martinez</name>
<name sortKey="Martins Silva, Leonardo" sort="Martins Silva, Leonardo" uniqKey="Martins Silva L" first="Leonardo" last="Martins-Silva">Leonardo Martins-Silva</name>
<name sortKey="Melo, Pollyana M S" sort="Melo, Pollyana M S" uniqKey="Melo P" first="Pollyana M. S." last="Melo">Pollyana M. S. Melo</name>
<name sortKey="Nagaoka, Marcia R" sort="Nagaoka, Marcia R" uniqKey="Nagaoka M" first="Marcia R." last="Nagaoka">Marcia R. Nagaoka</name>
<name sortKey="Pesquero, Joao B" sort="Pesquero, Joao B" uniqKey="Pesquero J" first="João B." last="Pesquero">João B. Pesquero</name>
</country>
</tree>
</affiliations>
</record>
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