Chloroquine is therapeutic in murine experimental model of paracoccidioidomycosis.
Identifieur interne : 000425 ( PubMed/Corpus ); précédent : 000424; suivant : 000426Chloroquine is therapeutic in murine experimental model of paracoccidioidomycosis.
Auteurs : Luciane Alarcão Dias-Melicio ; Sueli Aparecida Calvi ; Ana Paula Bordon ; Marjorie A. Golim ; Maria Terezinha Serrão Peraçoli ; Angela Maria Victoriano Campos SoaresSource :
- FEMS immunology and medical microbiology [ 0928-8244 ] ; 2007.
English descriptors
- KwdEn :
- Animals, Chloroquine (pharmacology), Disease Models, Animal, Hydrogen Peroxide (metabolism), Interleukin-6 (metabolism), Iron (metabolism), Macrophages, Peritoneal (drug effects), Macrophages, Peritoneal (immunology), Macrophages, Peritoneal (metabolism), Male, Mice, Mice, Inbred BALB C, Nitric Oxide (biosynthesis), Nitric Oxide (immunology), Paracoccidioides (isolation & purification), Paracoccidioidomycosis (drug therapy), Paracoccidioidomycosis (microbiology), Receptors, Transferrin (biosynthesis), Tumor Necrosis Factor-alpha (metabolism).
- MESH :
- chemical , biosynthesis : Nitric Oxide, Receptors, Transferrin.
- chemical , immunology : Nitric Oxide.
- chemical , metabolism : Hydrogen Peroxide, Interleukin-6, Iron, Tumor Necrosis Factor-alpha.
- chemical , pharmacology : Chloroquine.
- drug effects : Macrophages, Peritoneal.
- drug therapy : Paracoccidioidomycosis.
- immunology : Macrophages, Peritoneal.
- isolation & purification : Paracoccidioides.
- metabolism : Macrophages, Peritoneal.
- microbiology : Paracoccidioidomycosis.
- Animals, Disease Models, Animal, Male, Mice, Mice, Inbred BALB C.
Abstract
Chloroquine, due to its basic properties, has been shown to prevent the release of iron from holotransferrin, thereby interfering with normal iron metabolism in a variety of cell types. We have studied the effects of chloroquine on the evolution of experimental paracoccidioidomycosis by evaluating the viable fungal recovery from lung, liver and spleen from infected mice and H(2)O(2), NO production, tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-10 levels and transferrin receptor (TfR) expression from uninfected and infected peritoneal macrophages. Chloroquine caused a significant decrease in the viable fungal recovery from all organs tested, during all periods of evaluation. Peritoneal macrophages from chloroquine-treated infected mice showed higher H(2)O(2) production and TfR expression, and decreased levels of NO, endogenous and stimulated-TNF-alpha, IL-6 and IL-10 during the three evaluated periods. However, despite its suppressor effects on the macrophage function, the chloroquine therapeutic effect upon murine paracoccidioidomycosis was probably due to its effect on iron metabolism, blocking iron uptake by cells, and consequently restricting iron to fungus growth and survival.
DOI: 10.1111/j.1574-695X.2007.00243.x
PubMed: 17456179
Links to Exploration step
pubmed:17456179Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Chloroquine is therapeutic in murine experimental model of paracoccidioidomycosis.</title><author><name sortKey="Dias Melicio, Luciane Alarcao" sort="Dias Melicio, Luciane Alarcao" uniqKey="Dias Melicio L" first="Luciane Alarcão" last="Dias-Melicio">Luciane Alarcão Dias-Melicio</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Biosciences Institute, São Paulo State University, São Paulo, Brazil. ladiasmelicio@ibb.unesp.br</nlm:affiliation></affiliation></author><author><name sortKey="Calvi, Sueli Aparecida" sort="Calvi, Sueli Aparecida" uniqKey="Calvi S" first="Sueli Aparecida" last="Calvi">Sueli Aparecida Calvi</name></author><author><name sortKey="Bordon, Ana Paula" sort="Bordon, Ana Paula" uniqKey="Bordon A" first="Ana Paula" last="Bordon">Ana Paula Bordon</name></author><author><name sortKey="Golim, Marjorie A" sort="Golim, Marjorie A" uniqKey="Golim M" first="Marjorie A" last="Golim">Marjorie A. Golim</name></author><author><name sortKey="Peracoli, Maria Terezinha Serrao" sort="Peracoli, Maria Terezinha Serrao" uniqKey="Peracoli M" first="Maria Terezinha Serrão" last="Peraçoli">Maria Terezinha Serrão Peraçoli</name></author><author><name sortKey="Soares, Angela Maria Victoriano Campos" sort="Soares, Angela Maria Victoriano Campos" uniqKey="Soares A" first="Angela Maria Victoriano Campos" last="Soares">Angela Maria Victoriano Campos Soares</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2007">2007</date><idno type="RBID">pubmed:17456179</idno><idno type="pmid">17456179</idno><idno type="doi">10.1111/j.1574-695X.2007.00243.x</idno><idno type="wicri:Area/PubMed/Corpus">000425</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000425</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Chloroquine is therapeutic in murine experimental model of paracoccidioidomycosis.</title><author><name sortKey="Dias Melicio, Luciane Alarcao" sort="Dias Melicio, Luciane Alarcao" uniqKey="Dias Melicio L" first="Luciane Alarcão" last="Dias-Melicio">Luciane Alarcão Dias-Melicio</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Biosciences Institute, São Paulo State University, São Paulo, Brazil. ladiasmelicio@ibb.unesp.br</nlm:affiliation></affiliation></author><author><name sortKey="Calvi, Sueli Aparecida" sort="Calvi, Sueli Aparecida" uniqKey="Calvi S" first="Sueli Aparecida" last="Calvi">Sueli Aparecida Calvi</name></author><author><name sortKey="Bordon, Ana Paula" sort="Bordon, Ana Paula" uniqKey="Bordon A" first="Ana Paula" last="Bordon">Ana Paula Bordon</name></author><author><name sortKey="Golim, Marjorie A" sort="Golim, Marjorie A" uniqKey="Golim M" first="Marjorie A" last="Golim">Marjorie A. Golim</name></author><author><name sortKey="Peracoli, Maria Terezinha Serrao" sort="Peracoli, Maria Terezinha Serrao" uniqKey="Peracoli M" first="Maria Terezinha Serrão" last="Peraçoli">Maria Terezinha Serrão Peraçoli</name></author><author><name sortKey="Soares, Angela Maria Victoriano Campos" sort="Soares, Angela Maria Victoriano Campos" uniqKey="Soares A" first="Angela Maria Victoriano Campos" last="Soares">Angela Maria Victoriano Campos Soares</name></author></analytic><series><title level="j">FEMS immunology and medical microbiology</title><idno type="ISSN">0928-8244</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Chloroquine (pharmacology)</term><term>Disease Models, Animal</term><term>Hydrogen Peroxide (metabolism)</term><term>Interleukin-6 (metabolism)</term><term>Iron (metabolism)</term><term>Macrophages, Peritoneal (drug effects)</term><term>Macrophages, Peritoneal (immunology)</term><term>Macrophages, Peritoneal (metabolism)</term><term>Male</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Nitric Oxide (biosynthesis)</term><term>Nitric Oxide (immunology)</term><term>Paracoccidioides (isolation & purification)</term><term>Paracoccidioidomycosis (drug therapy)</term><term>Paracoccidioidomycosis (microbiology)</term><term>Receptors, Transferrin (biosynthesis)</term><term>Tumor Necrosis Factor-alpha (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Nitric Oxide</term><term>Receptors, Transferrin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Nitric Oxide</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Hydrogen Peroxide</term><term>Interleukin-6</term><term>Iron</term><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Macrophages, Peritoneal</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Paracoccidioidomycosis</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Macrophages, Peritoneal</term></keywords><keywords scheme="MESH" qualifier="isolation & purification" xml:lang="en"><term>Paracoccidioides</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Macrophages, Peritoneal</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Paracoccidioidomycosis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Male</term><term>Mice</term><term>Mice, Inbred BALB C</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Chloroquine, due to its basic properties, has been shown to prevent the release of iron from holotransferrin, thereby interfering with normal iron metabolism in a variety of cell types. We have studied the effects of chloroquine on the evolution of experimental paracoccidioidomycosis by evaluating the viable fungal recovery from lung, liver and spleen from infected mice and H(2)O(2), NO production, tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-10 levels and transferrin receptor (TfR) expression from uninfected and infected peritoneal macrophages. Chloroquine caused a significant decrease in the viable fungal recovery from all organs tested, during all periods of evaluation. Peritoneal macrophages from chloroquine-treated infected mice showed higher H(2)O(2) production and TfR expression, and decreased levels of NO, endogenous and stimulated-TNF-alpha, IL-6 and IL-10 during the three evaluated periods. However, despite its suppressor effects on the macrophage function, the chloroquine therapeutic effect upon murine paracoccidioidomycosis was probably due to its effect on iron metabolism, blocking iron uptake by cells, and consequently restricting iron to fungus growth and survival.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17456179</PMID><DateCompleted><Year>2007</Year><Month>10</Month><Day>04</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0928-8244</ISSN><JournalIssue CitedMedium="Print"><Volume>50</Volume><Issue>1</Issue><PubDate><Year>2007</Year><Month>Jun</Month></PubDate></JournalIssue><Title>FEMS immunology and medical microbiology</Title><ISOAbbreviation>FEMS Immunol. Med. Microbiol.</ISOAbbreviation></Journal><ArticleTitle>Chloroquine is therapeutic in murine experimental model of paracoccidioidomycosis.</ArticleTitle><Pagination><MedlinePgn>133-43</MedlinePgn></Pagination><Abstract><AbstractText>Chloroquine, due to its basic properties, has been shown to prevent the release of iron from holotransferrin, thereby interfering with normal iron metabolism in a variety of cell types. We have studied the effects of chloroquine on the evolution of experimental paracoccidioidomycosis by evaluating the viable fungal recovery from lung, liver and spleen from infected mice and H(2)O(2), NO production, tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-10 levels and transferrin receptor (TfR) expression from uninfected and infected peritoneal macrophages. Chloroquine caused a significant decrease in the viable fungal recovery from all organs tested, during all periods of evaluation. Peritoneal macrophages from chloroquine-treated infected mice showed higher H(2)O(2) production and TfR expression, and decreased levels of NO, endogenous and stimulated-TNF-alpha, IL-6 and IL-10 during the three evaluated periods. However, despite its suppressor effects on the macrophage function, the chloroquine therapeutic effect upon murine paracoccidioidomycosis was probably due to its effect on iron metabolism, blocking iron uptake by cells, and consequently restricting iron to fungus growth and survival.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dias-Melicio</LastName><ForeName>Luciane Alarcão</ForeName><Initials>LA</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Biosciences Institute, São Paulo State University, São Paulo, Brazil. ladiasmelicio@ibb.unesp.br</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Calvi</LastName><ForeName>Sueli Aparecida</ForeName><Initials>SA</Initials></Author><Author ValidYN="Y"><LastName>Bordon</LastName><ForeName>Ana Paula</ForeName><Initials>AP</Initials></Author><Author ValidYN="Y"><LastName>Golim</LastName><ForeName>Marjorie A</ForeName><Initials>MA</Initials></Author><Author ValidYN="Y"><LastName>Peraçoli</LastName><ForeName>Maria Terezinha Serrão</ForeName><Initials>MT</Initials></Author><Author ValidYN="Y"><LastName>Soares</LastName><ForeName>Angela Maria Victoriano Campos</ForeName><Initials>AM</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2007</Year><Month>04</Month><Day>23</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>FEMS Immunol Med Microbiol</MedlineTA><NlmUniqueID>9315554</NlmUniqueID><ISSNLinking>0928-8244</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015850">Interleukin-6</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011990">Receptors, Transferrin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance></Chemical><Chemical><RegistryNumber>31C4KY9ESH</RegistryNumber><NameOfSubstance UI="D009569">Nitric Oxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical><Chemical><RegistryNumber>BBX060AN9V</RegistryNumber><NameOfSubstance UI="D006861">Hydrogen Peroxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>E1UOL152H7</RegistryNumber><NameOfSubstance UI="D007501">Iron</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000494" 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MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009569" MajorTopicYN="N">Nitric Oxide</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010228" MajorTopicYN="N">Paracoccidioides</DescriptorName><QualifierName UI="Q000302" MajorTopicYN="Y">isolation & purification</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010229" MajorTopicYN="N">Paracoccidioidomycosis</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000382" 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