Chloroquine is therapeutic in murine experimental model of paracoccidioidomycosis.
Identifieur interne : 001A58 ( Main/Exploration ); précédent : 001A57; suivant : 001A59Chloroquine is therapeutic in murine experimental model of paracoccidioidomycosis.
Auteurs : Luciane Alarcão Dias-Melicio [Brésil] ; 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.
Descripteurs français
- KwdFr :
- Animaux, Blastomycose sud-américaine (microbiologie), Blastomycose sud-américaine (traitement médicamenteux), Chloroquine (pharmacologie), Facteur de nécrose tumorale alpha (métabolisme), Fer (métabolisme), Interleukine-6 (métabolisme), Macrophages péritonéaux (), Macrophages péritonéaux (immunologie), Macrophages péritonéaux (métabolisme), Modèles animaux de maladie humaine, Monoxyde d'azote (biosynthèse), Monoxyde d'azote (immunologie), Mâle, Paracoccidioides (isolement et purification), Peroxyde d'hydrogène (métabolisme), Récepteurs à la transferrine (biosynthèse), Souris, Souris de lignée BALB C.
- MESH :
- biosynthèse : Monoxyde d'azote, Récepteurs à la transferrine.
- immunologie : Macrophages péritonéaux, Monoxyde d'azote.
- isolement et purification : Paracoccidioides.
- microbiologie : Blastomycose sud-américaine.
- métabolisme : Facteur de nécrose tumorale alpha, Fer, Interleukine-6, Macrophages péritonéaux, Peroxyde d'hydrogène.
- pharmacologie : Chloroquine.
- traitement médicamenteux : Blastomycose sud-américaine.
- Animaux, Macrophages péritonéaux, Modèles animaux de maladie humaine, Mâle, Souris, Souris de lignée BALB C.
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
Affiliations:
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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><affiliations><list><country><li>Brésil</li></country><region><li>État de São Paulo</li></region><settlement><li>São Paulo</li></settlement></list><tree><noCountry><name sortKey="Bordon, Ana Paula" sort="Bordon, Ana Paula" uniqKey="Bordon A" first="Ana Paula" last="Bordon">Ana Paula Bordon</name><name sortKey="Calvi, Sueli Aparecida" sort="Calvi, Sueli Aparecida" uniqKey="Calvi S" first="Sueli Aparecida" last="Calvi">Sueli Aparecida Calvi</name><name sortKey="Golim, Marjorie A" sort="Golim, Marjorie A" uniqKey="Golim M" first="Marjorie A" last="Golim">Marjorie A. Golim</name><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><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></noCountry><country name="Brésil"><region name="État de São Paulo"><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></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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