ChloroquineV1, PascalFrancis, Corpus, bibRecord, 000036

Chloroquine is therapeutic in murine experimental model of paracoccidioidomycosis

Identifieur interne : 000036 ( PascalFrancis/Corpus ); précédent : 000035; suivant : 000037

Chloroquine is therapeutic in murine experimental model of paracoccidioidomycosis

Auteurs : Luciane Alarcao Dias-Melicio ; Sueli Aparecida Calvi ; Ana Paula Bordon ; Marjorie A. Golim ; Maria Terezinha Serrao Peracoli ; Angela Maria Victoriano Campos Soares

Source :

FEMS immunology and medical microbiology [ 0928-8244 ] ; 2007.

RBID : Pascal:07-0263607

Descripteurs français

Pascal (Inist)
- Blastomyces brasiliensis, Modèle animal, Fer, Hydrogène Peroxyde, Azote monoxyde, Cytokine, Microbiologie, Immunologie, Chloroquine, Paracoccidioïdomycose, Antiparasitaire, Antipaludique, Antirhumatismal.

English descriptors

KwdEn :
- Animal model, Antimalarial, Antirheumatic agent, Blastomyces brasiliensis, Chloroquine, Cytokine, Hydrogen Peroxides, Immunology, Iron, Microbiology, Nitric oxide, Paracoccidioidomycosis, Parasiticide.

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 H₂O_2, NO production, tumor necrosis factor-alpha (TNF-a), 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 H₂O₂ production and TfR expression, and decreased levels of NO, endogenous and stimulated-TNF-α, 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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A11	`02`	`1`		`@1 APARECIDA CALVI (Sueli)`
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A11	`04`	`1`		`@1 GOLIM (Marjorie A.)`
A11	`05`	`1`		`@1 SERRAO PERACOLI (Maria Terezinha)`
A11	`06`	`1`		`@1 CAMPOS SOARES (Angela Maria Victoriano)`
A14	`01`			`@1 Department of Microbiology and Immunology, Biosciences Institute, São Paulo State University @2 São Paulo @3 BRA @Z 1 aut. @Z 3 aut. @Z 5 aut. @Z 6 aut.`
A14	`02`			`@1 Department of Tropical Diseases, School of Medicine @2 São Paulo @3 BRA @Z 2 aut.`
A14	`03`			`@1 Botucatu Blood Center, School of Medicine, São Paulo State University @2 São Paulo @3 BRA @Z 4 aut.`
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C01	`01`		`ENG`	@0 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 H₂O_2, NO production, tumor necrosis factor-alpha (TNF-a), 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 H₂O₂ production and TfR expression, and decreased levels of NO, endogenous and stimulated-TNF-α, 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.
C02	`01`	`X`		`@0 002A05D10`
C02	`02`	`X`		`@0 002B05D02K1`
C03	`01`	`X`	`FRE`	`@0 Blastomyces brasiliensis @2 NS @5 01`
C03	`01`	`X`	`ENG`	`@0 Blastomyces brasiliensis @2 NS @5 01`
C03	`01`	`X`	`SPA`	`@0 Blastomyces brasiliensis @2 NS @5 01`
C03	`02`	`X`	`FRE`	`@0 Modèle animal @5 05`
C03	`02`	`X`	`ENG`	`@0 Animal model @5 05`
C03	`02`	`X`	`SPA`	`@0 Modelo animal @5 05`
C03	`03`	`X`	`FRE`	`@0 Fer @2 NC @5 06`
C03	`03`	`X`	`ENG`	`@0 Iron @2 NC @5 06`
C03	`03`	`X`	`SPA`	`@0 Hierro @2 NC @5 06`
C03	`04`	`X`	`FRE`	`@0 Hydrogène Peroxyde @2 NC @2 NA @5 07`
C03	`04`	`X`	`ENG`	`@0 Hydrogen Peroxides @2 NC @2 NA @5 07`
C03	`04`	`X`	`SPA`	`@0 Hidrógeno Peróxido @2 NC @2 NA @5 07`
C03	`05`	`X`	`FRE`	`@0 Azote monoxyde @2 NK @2 FX @5 08`
C03	`05`	`X`	`ENG`	`@0 Nitric oxide @2 NK @2 FX @5 08`
C03	`05`	`X`	`SPA`	`@0 Nitrógeno monóxido @2 NK @2 FX @5 08`
C03	`06`	`X`	`FRE`	`@0 Cytokine @5 09`
C03	`06`	`X`	`ENG`	`@0 Cytokine @5 09`
C03	`06`	`X`	`SPA`	`@0 Citoquina @5 09`
C03	`07`	`X`	`FRE`	`@0 Microbiologie @5 10`
C03	`07`	`X`	`ENG`	`@0 Microbiology @5 10`
C03	`07`	`X`	`SPA`	`@0 Microbiología @5 10`
C03	`08`	`X`	`FRE`	`@0 Immunologie @5 11`
C03	`08`	`X`	`ENG`	`@0 Immunology @5 11`
C03	`08`	`X`	`SPA`	`@0 Inmunología @5 11`
C03	`09`	`X`	`FRE`	`@0 Chloroquine @2 NK @2 FR @5 14`
C03	`09`	`X`	`ENG`	`@0 Chloroquine @2 NK @2 FR @5 14`
C03	`09`	`X`	`SPA`	`@0 Cloroquina @2 NK @2 FR @5 14`
C03	`10`	`X`	`FRE`	`@0 Paracoccidioïdomycose @5 15`
C03	`10`	`X`	`ENG`	`@0 Paracoccidioidomycosis @5 15`
C03	`10`	`X`	`SPA`	`@0 Paracoccidiomicosis @5 15`
C03	`11`	`X`	`FRE`	`@0 Antiparasitaire @5 45`
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C03	`11`	`X`	`SPA`	`@0 Antiparasitario @5 45`
C03	`12`	`X`	`FRE`	`@0 Antipaludique @5 46`
C03	`12`	`X`	`ENG`	`@0 Antimalarial @5 46`
C03	`12`	`X`	`SPA`	`@0 Antipalúdico @5 46`
C03	`13`	`X`	`FRE`	`@0 Antirhumatismal @5 54`
C03	`13`	`X`	`ENG`	`@0 Antirheumatic agent @5 54`
C03	`13`	`X`	`SPA`	`@0 Antireumático @5 54`
C07	`01`	`X`	`FRE`	`@0 Ascomycetes @2 NS`
C07	`01`	`X`	`ENG`	`@0 Ascomycetes @2 NS`
C07	`01`	`X`	`SPA`	`@0 Ascomycetes @2 NS`
C07	`02`	`X`	`FRE`	`@0 Fungi @2 NS`
C07	`02`	`X`	`ENG`	`@0 Fungi @2 NS`
C07	`02`	`X`	`SPA`	`@0 Fungi @2 NS`
C07	`03`	`X`	`FRE`	`@0 Thallophyta @2 NS`
C07	`03`	`X`	`ENG`	`@0 Thallophyta @2 NS`
C07	`03`	`X`	`SPA`	`@0 Thallophyta @2 NS`
C07	`04`	`X`	`FRE`	`@0 Blastomycose`
C07	`04`	`X`	`ENG`	`@0 Blastomycosis`
C07	`04`	`X`	`SPA`	`@0 Blastomicosis`
C07	`05`	`X`	`FRE`	`@0 Mycose`
C07	`05`	`X`	`ENG`	`@0 Mycosis`
C07	`05`	`X`	`SPA`	`@0 Micosis`
C07	`06`	`X`	`FRE`	`@0 Infection`
C07	`06`	`X`	`ENG`	`@0 Infection`
C07	`06`	`X`	`SPA`	`@0 Infección`
N21				`@1 176`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 07-0263607 INIST
ET :	Chloroquine is therapeutic in murine experimental model of paracoccidioidomycosis
AU :	ALARCAO DIAS-MELICIO (Luciane); APARECIDA CALVI (Sueli); BORDON (Ana Paula); GOLIM (Marjorie A.); SERRAO PERACOLI (Maria Terezinha); CAMPOS SOARES (Angela Maria Victoriano)
AF :	Department of Microbiology and Immunology, Biosciences Institute, São Paulo State University/São Paulo/Brésil (1 aut., 3 aut., 5 aut., 6 aut.); Department of Tropical Diseases, School of Medicine/São Paulo/Brésil (2 aut.); Botucatu Blood Center, School of Medicine, São Paulo State University/São Paulo/Brésil (4 aut.)
DT :	Publication en série; Niveau analytique
SO :	FEMS immunology and medical microbiology; ISSN 0928-8244; Royaume-Uni; Da. 2007; Vol. 50; No. 1; Pp. 133-143; Bibl. 2 p.1/2
LA :	Anglais
EA :	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 H₂O_2, NO production, tumor necrosis factor-alpha (TNF-a), 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 H₂O₂ production and TfR expression, and decreased levels of NO, endogenous and stimulated-TNF-α, 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.
CC :	002A05D10; 002B05D02K1
FD :	Blastomyces brasiliensis; Modèle animal; Fer; Hydrogène Peroxyde; Azote monoxyde; Cytokine; Microbiologie; Immunologie; Chloroquine; Paracoccidioïdomycose; Antiparasitaire; Antipaludique; Antirhumatismal
FG :	Ascomycetes; Fungi; Thallophyta; Blastomycose; Mycose; Infection
ED :	Blastomyces brasiliensis; Animal model; Iron; Hydrogen Peroxides; Nitric oxide; Cytokine; Microbiology; Immunology; Chloroquine; Paracoccidioidomycosis; Parasiticide; Antimalarial; Antirheumatic agent
EG :	Ascomycetes; Fungi; Thallophyta; Blastomycosis; Mycosis; Infection
SD :	Blastomyces brasiliensis; Modelo animal; Hierro; Hidrógeno Peróxido; Nitrógeno monóxido; Citoquina; Microbiología; Inmunología; Cloroquina; Paracoccidiomicosis; Antiparasitario; Antipalúdico; Antireumático
LO :	INIST-17567B.354000149579490150
ID :	07-0263607

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Pascal:07-0263607

Le document en format XML

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<term>Chloroquine</term>
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<term>Hydrogen Peroxides</term>
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<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<sub>2</sub>
O<sub>2,</sub>
 NO production, tumor necrosis factor-alpha (TNF-a), 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<sub>2</sub>
O<sub>2</sub>
 production and TfR expression, and decreased levels of NO, endogenous and stimulated-TNF-α, 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>
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<fA11 i1="01" i2="1"><s1>ALARCAO DIAS-MELICIO (Luciane)</s1>
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<fA14 i1="01"><s1>Department of Microbiology and Immunology, Biosciences Institute, São Paulo State University</s1>
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<fA14 i1="02"><s1>Department of Tropical Diseases, School of Medicine</s1>
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<s3>BRA</s3>
<sZ>2 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Botucatu Blood Center, School of Medicine, São Paulo State University</s1>
<s2>São Paulo</s2>
<s3>BRA</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA20><s1>133-143</s1>
</fA20>
<fA21><s1>2007</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>17567B</s2>
<s5>354000149579490150</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2007 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>2 p.1/2</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>07-0263607</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>FEMS immunology and medical microbiology</s0>
</fA64>
<fA66 i1="01"><s0>GBR</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>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<sub>2</sub>
O<sub>2,</sub>
 NO production, tumor necrosis factor-alpha (TNF-a), 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<sub>2</sub>
O<sub>2</sub>
 production and TfR expression, and decreased levels of NO, endogenous and stimulated-TNF-α, 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.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A05D10</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B05D02K1</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Blastomyces brasiliensis</s0>
<s2>NS</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Blastomyces brasiliensis</s0>
<s2>NS</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Blastomyces brasiliensis</s0>
<s2>NS</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Modèle animal</s0>
<s5>05</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Animal model</s0>
<s5>05</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Modelo animal</s0>
<s5>05</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Fer</s0>
<s2>NC</s2>
<s5>06</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Iron</s0>
<s2>NC</s2>
<s5>06</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Hierro</s0>
<s2>NC</s2>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Hydrogène Peroxyde</s0>
<s2>NC</s2>
<s2>NA</s2>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Hydrogen Peroxides</s0>
<s2>NC</s2>
<s2>NA</s2>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Hidrógeno Peróxido</s0>
<s2>NC</s2>
<s2>NA</s2>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Azote monoxyde</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>08</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Nitric oxide</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>08</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Nitrógeno monóxido</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Cytokine</s0>
<s5>09</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Cytokine</s0>
<s5>09</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Citoquina</s0>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Microbiologie</s0>
<s5>10</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Microbiology</s0>
<s5>10</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Microbiología</s0>
<s5>10</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Immunologie</s0>
<s5>11</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Immunology</s0>
<s5>11</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Inmunología</s0>
<s5>11</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Chloroquine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Chloroquine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Cloroquina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>14</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Paracoccidioïdomycose</s0>
<s5>15</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Paracoccidioidomycosis</s0>
<s5>15</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Paracoccidiomicosis</s0>
<s5>15</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Antiparasitaire</s0>
<s5>45</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Parasiticide</s0>
<s5>45</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Antiparasitario</s0>
<s5>45</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Antipaludique</s0>
<s5>46</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Antimalarial</s0>
<s5>46</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Antipalúdico</s0>
<s5>46</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE"><s0>Antirhumatismal</s0>
<s5>54</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG"><s0>Antirheumatic agent</s0>
<s5>54</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA"><s0>Antireumático</s0>
<s5>54</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Ascomycetes</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Ascomycetes</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Ascomycetes</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Fungi</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Fungi</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Fungi</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Thallophyta</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Thallophyta</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Thallophyta</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Blastomycose</s0>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Blastomycosis</s0>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Blastomicosis</s0>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Mycose</s0>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Mycosis</s0>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Micosis</s0>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<fN21><s1>176</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 07-0263607 INIST</NO>
<ET>Chloroquine is therapeutic in murine experimental model of paracoccidioidomycosis</ET>
<AU>ALARCAO DIAS-MELICIO (Luciane); APARECIDA CALVI (Sueli); BORDON (Ana Paula); GOLIM (Marjorie A.); SERRAO PERACOLI (Maria Terezinha); CAMPOS SOARES (Angela Maria Victoriano)</AU>
<AF>Department of Microbiology and Immunology, Biosciences Institute, São Paulo State University/São Paulo/Brésil (1 aut., 3 aut., 5 aut., 6 aut.); Department of Tropical Diseases, School of Medicine/São Paulo/Brésil (2 aut.); Botucatu Blood Center, School of Medicine, São Paulo State University/São Paulo/Brésil (4 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>FEMS immunology and medical microbiology; ISSN 0928-8244; Royaume-Uni; Da. 2007; Vol. 50; No. 1; Pp. 133-143; Bibl. 2 p.1/2</SO>
<LA>Anglais</LA>
<EA>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<sub>2</sub>
O<sub>2,</sub>
 NO production, tumor necrosis factor-alpha (TNF-a), 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<sub>2</sub>
O<sub>2</sub>
 production and TfR expression, and decreased levels of NO, endogenous and stimulated-TNF-α, 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.</EA>
<CC>002A05D10; 002B05D02K1</CC>
<FD>Blastomyces brasiliensis; Modèle animal; Fer; Hydrogène Peroxyde; Azote monoxyde; Cytokine; Microbiologie; Immunologie; Chloroquine; Paracoccidioïdomycose; Antiparasitaire; Antipaludique; Antirhumatismal</FD>
<FG>Ascomycetes; Fungi; Thallophyta; Blastomycose; Mycose; Infection</FG>
<ED>Blastomyces brasiliensis; Animal model; Iron; Hydrogen Peroxides; Nitric oxide; Cytokine; Microbiology; Immunology; Chloroquine; Paracoccidioidomycosis; Parasiticide; Antimalarial; Antirheumatic agent</ED>
<EG>Ascomycetes; Fungi; Thallophyta; Blastomycosis; Mycosis; Infection</EG>
<SD>Blastomyces brasiliensis; Modelo animal; Hierro; Hidrógeno Peróxido; Nitrógeno monóxido; Citoquina; Microbiología; Inmunología; Cloroquina; Paracoccidiomicosis; Antiparasitario; Antipalúdico; Antireumático</SD>
<LO>INIST-17567B.354000149579490150</LO>
<ID>07-0263607</ID>
</server>
</inist>
</record>

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Chloroquine is therapeutic in murine experimental model of paracoccidioidomycosis

Chloroquine is therapeutic in murine experimental model of paracoccidioidomycosis

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