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1
Restrepo-Moreno A, 2003. Paracoccidioidomycosis. Deismukes WE, Pappas PG, Sobel JD, eds. Clinical Mycology. New York: Oxford University Press, 328–345.
-
2
Green SJ, Meltzer MS, Hibbs JB Jr, Nacy CA, 1990. Activated macrophages destroy intracellular Leishmania major amastigottes by an L-arginine-dependent killing mechanism. J Immunol 144 :278–283.
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3
González A, De Gregori W, Vélez D, Restrepo A, Cano LE, 2000. Nitric oxide participation in the fungicidal mechanism of gamma interferon-activated murine macrophages against Paracoccidioides brasiliensis conidia. Infect Immun 68 :2546–2552.
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4
Brummer E, Hanson LH, Stevens DA, 1988. Gamma interferon activation of macrophages for killing of Paracoccidioides brasiliensis and evidence for nonoxidative mechanism. Int J Immunopharmacol 10 :945–952.
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5
Louie A, Baltch AL, Smith RP, Franke MA, Ritz WJ, Singh JK, Gordon MA, 1994. Tumor necrosis factor alpha has a protective role in murine model of systemic candidiasis. Infect Immun 62 :2761–2772.
-
6
Smith JG, Magee DM, Williams DM, Graybill JR, 1990. Tumor necrosis factor alpha plays a role in host defense against Histoplasma capsulatum.J Infect Dis 162 :1349–1353.
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7
Restrepo A, Jiménez BE, 1980. Growth of Paracoccidioides brasiliensis yeast phase in to chemical defined culture medium. J Clin Microbiol 12 :279–281.
-
8
Restrepo A, Salazar ME, Cano LE, Patiño ME, 1986. A technique to collect and dislodge conidia produced by Paracoccidioides brasiliensis mycelial form. J Med Vet Mycol 24 :247–250.
-
9
Ding AH, Nathan CF, Sturh DJ, 1988. Release of reactive nitrogen intermediates and it reactivates oxygen intermediates from mouse peritoneal macrophages. J Immunol 141 :2407–2412.
-
10
Liew FY, Li Y, Millot S, 1990. Tumor necrosis factor-α synergizes with IFN-γ in mediating killing of Leishmania major through the induction of nitric oxide. J Immunol 145 :4305–4310.
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11
Silva JS, Vespa GNR, Cardoso MAG, Aliberti JCS, Cunha FQ, 1995. Tumor necrosis factor alpha mediates resistance to Trypanosoma cruzi infection in mice by inducing nitric oxide production in infected gamma-interferon-activated macrophages. Infect Immun 63 :4862–4867.
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12
Fonseca SG, Romao PRT, Figueiredo F, Morais RH, Lima HC, Ferreria SH, Cunha FQ, 2003. TNF-α mediates the induction of nitric oxide synthase in macrophages but not in neutrophils in experimental cutaneous leishmaniasis. Eur J immunol 33 :2297–2306.
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13
González A, Caro E, Aristizábal BH, Restrepo A, Cano LE, 2003. Expression of iNOS and NFκB in peritoneal macrophages activated with IFN-γ. Annu Rev Biomed Sci 4 :133–139.
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14
Dorger M, Jesch NK, Rieder G, Hirvonen MR, Savolainen K, Krombach F, Messmer K, 1997. Species differences in NO formation by rat and hamster alveolar macrophages in vitro.Am J Respir Cell Mol Biol 16 :413–420.
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15
Paris-Fortes MR, da Silva MF, Sugizaki MF, Defaveri J, Montenegro MR, Soares AMVC, Peraçoli MTS, 2000. Experimental Paracoccidioidomycosis of the Syrian hamster: fungicidal activity and production of inflammatory cytokines by macrophages. Med Mycol 38 :51–60.
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16
Souto JT, Figueriedo F, Furlanetto A, Pfeffer K, Rossi MA, Silva JS, 2000. Interferon-gamma and tumor necrosis factor-alpha determine resistance to Paracoccidioides brasiliensis infection mice. Am J Pathol 156 :1811–1820.
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17
Calich VL, Kashino SS, 1998. Cytokines produced by susceptible and resistant mice in the course of Paracoccidioides brasiliensis infection. Braz J Med Biol Res 31 :615–623.
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18
Bocca AL, Hayashi EE, Pinheiro AG, Furlanetto AB, Campanelli AP, Cunha FQ, Figueiredo F, 1998. Treatment of Paracoccidioides brasiliensis-infected mice with a nitric oxide inhibitor prevents the failure of cell-mediated immune response. J Immunol 161 :3056–3063.
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19
Nascimento FRF, Calich VLG, Rodriguez D, Russo M, 2002. Dual role for nitric oxide in paracoccidioidomycosis: essential for resistance, but overproduction associated with susceptibility. J Immunol 168 :4593–4600.
| Past two years | Past Year | Past 30 Days | |
|---|---|---|---|
| Abstract Views | 52 | 28 | 3 |
| Full Text Views | 198 | 4 | 1 |
| PDF Downloads | 36 | 4 | 1 |
SHORT REPORT: INHIBITION BY TUMOR NECROSIS FACTOR-α–ACTIVATED MACROPHAGES OF THE TRANSITION OF PARACOCCIDIOIDES BRASILIENSIS CONIDIA TO YEAST CELLS THROUGH A MECHANISM INDEPENDENT OF NITRIC OXIDE
ANGEL GONZALEZ
ANGEL GONZALEZ
Medical and Experimental Mycology Group, Corporación para Investigaciones Biológicas, Medellín, Colombia; Molecular Microbiology Group, Clinical Laboratory and Bacteriology School, Universidad de Antioquia, Medellín, Colombia
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BEATRIZ H. ARISTIZÁBAL
BEATRIZ H. ARISTIZÁBAL
Medical and Experimental Mycology Group, Corporación para Investigaciones Biológicas, Medellín, Colombia; Molecular Microbiology Group, Clinical Laboratory and Bacteriology School, Universidad de Antioquia, Medellín, Colombia
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ERIKA CARO GÓMEZ
ERIKA CARO GÓMEZ
Medical and Experimental Mycology Group, Corporación para Investigaciones Biológicas, Medellín, Colombia; Molecular Microbiology Group, Clinical Laboratory and Bacteriology School, Universidad de Antioquia, Medellín, Colombia
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ANGELA RESTREPO
ANGELA RESTREPO
Medical and Experimental Mycology Group, Corporación para Investigaciones Biológicas, Medellín, Colombia; Molecular Microbiology Group, Clinical Laboratory and Bacteriology School, Universidad de Antioquia, Medellín, Colombia
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LUZ E. CANO
LUZ E. CANO
Medical and Experimental Mycology Group, Corporación para Investigaciones Biológicas, Medellín, Colombia; Molecular Microbiology Group, Clinical Laboratory and Bacteriology School, Universidad de Antioquia, Medellín, Colombia
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It is known that peritoneal murine macrophages activated with interferon-γ exert a fungicidal effect against Paracoccidioides brasiliensis conidia by a nitric oxide (NO)-mediated mechanism. This NO-mediated effect can also be induced by other cytokines such as tumor necrosis factor-α (TNF-α). The aim of this study was to determine if TNF-α-activated peritoneal murine macrophages infected with P. brasiliensis were able to show fungistatic/fungicidal effects mediated by NO. The results indicated that although macrophage activation with TNF-α did not result in NO production, these cells played an important role in inhibiting the conidia from becoming yeast cells. In vivo, the NO-independent inhibitory effect would prove of importance for the establishment of P. brasiliensis in host tissues.
Author Notes
ProCite
RefWorks
Reference Manager
BibTeX
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-
1
Restrepo-Moreno A, 2003. Paracoccidioidomycosis. Deismukes WE, Pappas PG, Sobel JD, eds. Clinical Mycology. New York: Oxford University Press, 328–345.
-
2
Green SJ, Meltzer MS, Hibbs JB Jr, Nacy CA, 1990. Activated macrophages destroy intracellular Leishmania major amastigottes by an L-arginine-dependent killing mechanism. J Immunol 144 :278–283.
-
3
González A, De Gregori W, Vélez D, Restrepo A, Cano LE, 2000. Nitric oxide participation in the fungicidal mechanism of gamma interferon-activated murine macrophages against Paracoccidioides brasiliensis conidia. Infect Immun 68 :2546–2552.
-
4
Brummer E, Hanson LH, Stevens DA, 1988. Gamma interferon activation of macrophages for killing of Paracoccidioides brasiliensis and evidence for nonoxidative mechanism. Int J Immunopharmacol 10 :945–952.
-
5
Louie A, Baltch AL, Smith RP, Franke MA, Ritz WJ, Singh JK, Gordon MA, 1994. Tumor necrosis factor alpha has a protective role in murine model of systemic candidiasis. Infect Immun 62 :2761–2772.
-
6
Smith JG, Magee DM, Williams DM, Graybill JR, 1990. Tumor necrosis factor alpha plays a role in host defense against Histoplasma capsulatum.J Infect Dis 162 :1349–1353.
-
7
Restrepo A, Jiménez BE, 1980. Growth of Paracoccidioides brasiliensis yeast phase in to chemical defined culture medium. J Clin Microbiol 12 :279–281.
-
8
Restrepo A, Salazar ME, Cano LE, Patiño ME, 1986. A technique to collect and dislodge conidia produced by Paracoccidioides brasiliensis mycelial form. J Med Vet Mycol 24 :247–250.
-
9
Ding AH, Nathan CF, Sturh DJ, 1988. Release of reactive nitrogen intermediates and it reactivates oxygen intermediates from mouse peritoneal macrophages. J Immunol 141 :2407–2412.
-
10
Liew FY, Li Y, Millot S, 1990. Tumor necrosis factor-α synergizes with IFN-γ in mediating killing of Leishmania major through the induction of nitric oxide. J Immunol 145 :4305–4310.
-
11
Silva JS, Vespa GNR, Cardoso MAG, Aliberti JCS, Cunha FQ, 1995. Tumor necrosis factor alpha mediates resistance to Trypanosoma cruzi infection in mice by inducing nitric oxide production in infected gamma-interferon-activated macrophages. Infect Immun 63 :4862–4867.
-
12
Fonseca SG, Romao PRT, Figueiredo F, Morais RH, Lima HC, Ferreria SH, Cunha FQ, 2003. TNF-α mediates the induction of nitric oxide synthase in macrophages but not in neutrophils in experimental cutaneous leishmaniasis. Eur J immunol 33 :2297–2306.
-
13
González A, Caro E, Aristizábal BH, Restrepo A, Cano LE, 2003. Expression of iNOS and NFκB in peritoneal macrophages activated with IFN-γ. Annu Rev Biomed Sci 4 :133–139.
-
14
Dorger M, Jesch NK, Rieder G, Hirvonen MR, Savolainen K, Krombach F, Messmer K, 1997. Species differences in NO formation by rat and hamster alveolar macrophages in vitro.Am J Respir Cell Mol Biol 16 :413–420.
-
15
Paris-Fortes MR, da Silva MF, Sugizaki MF, Defaveri J, Montenegro MR, Soares AMVC, Peraçoli MTS, 2000. Experimental Paracoccidioidomycosis of the Syrian hamster: fungicidal activity and production of inflammatory cytokines by macrophages. Med Mycol 38 :51–60.
-
16
Souto JT, Figueriedo F, Furlanetto A, Pfeffer K, Rossi MA, Silva JS, 2000. Interferon-gamma and tumor necrosis factor-alpha determine resistance to Paracoccidioides brasiliensis infection mice. Am J Pathol 156 :1811–1820.
-
17
Calich VL, Kashino SS, 1998. Cytokines produced by susceptible and resistant mice in the course of Paracoccidioides brasiliensis infection. Braz J Med Biol Res 31 :615–623.
-
18
Bocca AL, Hayashi EE, Pinheiro AG, Furlanetto AB, Campanelli AP, Cunha FQ, Figueiredo F, 1998. Treatment of Paracoccidioides brasiliensis-infected mice with a nitric oxide inhibitor prevents the failure of cell-mediated immune response. J Immunol 161 :3056–3063.
-
19
Nascimento FRF, Calich VLG, Rodriguez D, Russo M, 2002. Dual role for nitric oxide in paracoccidioidomycosis: essential for resistance, but overproduction associated with susceptibility. J Immunol 168 :4593–4600.
| Past two years | Past Year | Past 30 Days | |
|---|---|---|---|
| Abstract Views | 52 | 28 | 3 |
| Full Text Views | 198 | 4 | 1 |
| PDF Downloads | 36 | 4 | 1 |