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Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism.
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Zeitschriftentitel: | The Journal of experimental medicine |
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Personen und Körperschaften: | , , , |
In: | The Journal of experimental medicine, 180, 1994, 1, S. 365-369 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
Rockefeller University Press
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Schlagwörter: |
author_facet |
Lee, S C Dickson, D W Brosnan, C F Casadevall, A Lee, S C Dickson, D W Brosnan, C F Casadevall, A |
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author |
Lee, S C Dickson, D W Brosnan, C F Casadevall, A |
spellingShingle |
Lee, S C Dickson, D W Brosnan, C F Casadevall, A The Journal of experimental medicine Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism. Immunology Immunology and Allergy |
author_sort |
lee, s c |
spelling |
Lee, S C Dickson, D W Brosnan, C F Casadevall, A 0022-1007 1540-9538 Rockefeller University Press Immunology Immunology and Allergy http://dx.doi.org/10.1084/jem.180.1.365 <jats:p>Cryptococcus neoformans is an opportunistic fungus that causes life-threatening meningoencephalitis in 5-10% of patients with acquired immune deficiency syndrome. Cryptococcal meningoencephalitis is characterized by a lymphohistiocytic infiltrate, accumulation of encapsulated forms of C. neoformans, and varying degrees of glial reaction. Little is known about the contribution of endogenous central nervous system cells to the pathogenesis of cryptococcal infections. In this study, we investigated the role of astrocytes as potential effector cells against C. neoformans. Primary cultures of human fetal astrocytes, activated with interleukin 1 beta plus interferon gamma inhibited the growth of C. neoformans. The inhibition of C. neoformans growth was paralleled by production of nitrite, and reversed by the inhibitors of nitric oxide (NO.) synthase, NG-methyl-mono-arginine and NG-nitro-arginine methyl ester. The results suggest a novel function for human astrocytes in host defence and provide a precedent for the use of NO. as an antimicrobial effector molecule by human cells.</jats:p> Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism. The Journal of experimental medicine |
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Rockefeller University Press, 1994 |
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Rockefeller University Press |
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The Journal of experimental medicine |
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title |
Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism. |
title_unstemmed |
Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism. |
title_full |
Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism. |
title_fullStr |
Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism. |
title_full_unstemmed |
Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism. |
title_short |
Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism. |
title_sort |
human astrocytes inhibit cryptococcus neoformans growth by a nitric oxide-mediated mechanism. |
topic |
Immunology Immunology and Allergy |
url |
http://dx.doi.org/10.1084/jem.180.1.365 |
publishDate |
1994 |
physical |
365-369 |
description |
<jats:p>Cryptococcus neoformans is an opportunistic fungus that causes life-threatening meningoencephalitis in 5-10% of patients with acquired immune deficiency syndrome. Cryptococcal meningoencephalitis is characterized by a lymphohistiocytic infiltrate, accumulation of encapsulated forms of C. neoformans, and varying degrees of glial reaction. Little is known about the contribution of endogenous central nervous system cells to the pathogenesis of cryptococcal infections. In this study, we investigated the role of astrocytes as potential effector cells against C. neoformans. Primary cultures of human fetal astrocytes, activated with interleukin 1 beta plus interferon gamma inhibited the growth of C. neoformans. The inhibition of C. neoformans growth was paralleled by production of nitrite, and reversed by the inhibitors of nitric oxide (NO.) synthase, NG-methyl-mono-arginine and NG-nitro-arginine methyl ester. The results suggest a novel function for human astrocytes in host defence and provide a precedent for the use of NO. as an antimicrobial effector molecule by human cells.</jats:p> |
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author | Lee, S C, Dickson, D W, Brosnan, C F, Casadevall, A |
author_facet | Lee, S C, Dickson, D W, Brosnan, C F, Casadevall, A, Lee, S C, Dickson, D W, Brosnan, C F, Casadevall, A |
author_sort | lee, s c |
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description | <jats:p>Cryptococcus neoformans is an opportunistic fungus that causes life-threatening meningoencephalitis in 5-10% of patients with acquired immune deficiency syndrome. Cryptococcal meningoencephalitis is characterized by a lymphohistiocytic infiltrate, accumulation of encapsulated forms of C. neoformans, and varying degrees of glial reaction. Little is known about the contribution of endogenous central nervous system cells to the pathogenesis of cryptococcal infections. In this study, we investigated the role of astrocytes as potential effector cells against C. neoformans. Primary cultures of human fetal astrocytes, activated with interleukin 1 beta plus interferon gamma inhibited the growth of C. neoformans. The inhibition of C. neoformans growth was paralleled by production of nitrite, and reversed by the inhibitors of nitric oxide (NO.) synthase, NG-methyl-mono-arginine and NG-nitro-arginine methyl ester. The results suggest a novel function for human astrocytes in host defence and provide a precedent for the use of NO. as an antimicrobial effector molecule by human cells.</jats:p> |
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spelling | Lee, S C Dickson, D W Brosnan, C F Casadevall, A 0022-1007 1540-9538 Rockefeller University Press Immunology Immunology and Allergy http://dx.doi.org/10.1084/jem.180.1.365 <jats:p>Cryptococcus neoformans is an opportunistic fungus that causes life-threatening meningoencephalitis in 5-10% of patients with acquired immune deficiency syndrome. Cryptococcal meningoencephalitis is characterized by a lymphohistiocytic infiltrate, accumulation of encapsulated forms of C. neoformans, and varying degrees of glial reaction. Little is known about the contribution of endogenous central nervous system cells to the pathogenesis of cryptococcal infections. In this study, we investigated the role of astrocytes as potential effector cells against C. neoformans. Primary cultures of human fetal astrocytes, activated with interleukin 1 beta plus interferon gamma inhibited the growth of C. neoformans. The inhibition of C. neoformans growth was paralleled by production of nitrite, and reversed by the inhibitors of nitric oxide (NO.) synthase, NG-methyl-mono-arginine and NG-nitro-arginine methyl ester. The results suggest a novel function for human astrocytes in host defence and provide a precedent for the use of NO. as an antimicrobial effector molecule by human cells.</jats:p> Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism. The Journal of experimental medicine |
spellingShingle | Lee, S C, Dickson, D W, Brosnan, C F, Casadevall, A, The Journal of experimental medicine, Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism., Immunology, Immunology and Allergy |
title | Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism. |
title_full | Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism. |
title_fullStr | Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism. |
title_full_unstemmed | Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism. |
title_short | Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism. |
title_sort | human astrocytes inhibit cryptococcus neoformans growth by a nitric oxide-mediated mechanism. |
title_unstemmed | Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism. |
topic | Immunology, Immunology and Allergy |
url | http://dx.doi.org/10.1084/jem.180.1.365 |