Biological Response Modifiers and Parasitic Infections: Experimental Aspects of Toxoplasmosis

Parasitic infections are important causes of disease in the developing world and, since the advent of AIDS, the developed world. Over the past decade, in vitro and in vivo studies have established the important role that biological response modifiers play in pathogenesis of parasitic disease. These...

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Main Author: Miles H Beaman
Format: Article
Language:English
Published: Hindawi Limited 1994-01-01
Series:Canadian Journal of Infectious Diseases
Online Access:http://dx.doi.org/10.1155/1994/712364
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spelling doaj-ce1e864ace714262a4abaef639ce092f2020-11-24T21:35:41ZengHindawi LimitedCanadian Journal of Infectious Diseases1180-23321994-01-015Suppl A47A50A10.1155/1994/712364Biological Response Modifiers and Parasitic Infections: Experimental Aspects of ToxoplasmosisMiles H Beaman0University of Western Australia and Fremantle Hospital, Perth, Western Australia, AustraliaParasitic infections are important causes of disease in the developing world and, since the advent of AIDS, the developed world. Over the past decade, in vitro and in vivo studies have established the important role that biological response modifiers play in pathogenesis of parasitic disease. These basic studies have resulted in successful clinical trials of interferon gamma (IFN-γ) in human leishmaniasis. Toxoplasmic encephalitis is a major opportunistic infection in patients with AIDS. and current therapy is often problematic. IFN-γ has been shown in in vitro and in vivo animal studies to be critical for host defence against Toxoplasma gondii. Tumour necrosis factor alpha plays a critical role in mediating IFN-γ effect in vitro, but its role in vivo is under further study. lnterleukin (1L)-6 and IL-10 have both recently been shown to enhance T gondii replication in vitro and to antagonize the beneficial effects of IPN-γ. In addition, in certain mouse strains. IL-6 has been shown to worsen mortality from T gondii infection. Future strategies for therapy of T gondii may include administration of exogenous IFN-γ or IL-12 with or without antibody to antagonistic cytokines such as IL-6 (or possibly IL-10).http://dx.doi.org/10.1155/1994/712364
collection DOAJ
language English
format Article
sources DOAJ
author Miles H Beaman
spellingShingle Miles H Beaman
Biological Response Modifiers and Parasitic Infections: Experimental Aspects of Toxoplasmosis
Canadian Journal of Infectious Diseases
author_facet Miles H Beaman
author_sort Miles H Beaman
title Biological Response Modifiers and Parasitic Infections: Experimental Aspects of Toxoplasmosis
title_short Biological Response Modifiers and Parasitic Infections: Experimental Aspects of Toxoplasmosis
title_full Biological Response Modifiers and Parasitic Infections: Experimental Aspects of Toxoplasmosis
title_fullStr Biological Response Modifiers and Parasitic Infections: Experimental Aspects of Toxoplasmosis
title_full_unstemmed Biological Response Modifiers and Parasitic Infections: Experimental Aspects of Toxoplasmosis
title_sort biological response modifiers and parasitic infections: experimental aspects of toxoplasmosis
publisher Hindawi Limited
series Canadian Journal of Infectious Diseases
issn 1180-2332
publishDate 1994-01-01
description Parasitic infections are important causes of disease in the developing world and, since the advent of AIDS, the developed world. Over the past decade, in vitro and in vivo studies have established the important role that biological response modifiers play in pathogenesis of parasitic disease. These basic studies have resulted in successful clinical trials of interferon gamma (IFN-γ) in human leishmaniasis. Toxoplasmic encephalitis is a major opportunistic infection in patients with AIDS. and current therapy is often problematic. IFN-γ has been shown in in vitro and in vivo animal studies to be critical for host defence against Toxoplasma gondii. Tumour necrosis factor alpha plays a critical role in mediating IFN-γ effect in vitro, but its role in vivo is under further study. lnterleukin (1L)-6 and IL-10 have both recently been shown to enhance T gondii replication in vitro and to antagonize the beneficial effects of IPN-γ. In addition, in certain mouse strains. IL-6 has been shown to worsen mortality from T gondii infection. Future strategies for therapy of T gondii may include administration of exogenous IFN-γ or IL-12 with or without antibody to antagonistic cytokines such as IL-6 (or possibly IL-10).
url http://dx.doi.org/10.1155/1994/712364
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