Human malarial disease: a consequence of inflammatory cytokine release
Abstract Malaria causes an acute systemic human disease that bears many similarities, both clinically and mechanistically, to those caused by bacteria, rickettsia, and viruses. Over the past few decades, a literature has emerged that argues for most of the pathology seen in all of these infectious d...
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ftdoajarticles:oai:doaj.org/article:433348442d4b4f0aa435971c1df9ff3a 2023-05-15T15:08:23+02:00 Human malarial disease: a consequence of inflammatory cytokine release Alleva Lisa M Budd Alison C Clark Ian A Cowden William B 2006-10-01T00:00:00Z https://doi.org/10.1186/1475-2875-5-85 https://doaj.org/article/433348442d4b4f0aa435971c1df9ff3a EN eng BMC http://www.malariajournal.com/content/5/1/85 https://doaj.org/toc/1475-2875 doi:10.1186/1475-2875-5-85 1475-2875 https://doaj.org/article/433348442d4b4f0aa435971c1df9ff3a Malaria Journal, Vol 5, Iss 1, p 85 (2006) Arctic medicine. Tropical medicine RC955-962 Infectious and parasitic diseases RC109-216 article 2006 ftdoajarticles https://doi.org/10.1186/1475-2875-5-85 2022-12-31T08:12:27Z Abstract Malaria causes an acute systemic human disease that bears many similarities, both clinically and mechanistically, to those caused by bacteria, rickettsia, and viruses. Over the past few decades, a literature has emerged that argues for most of the pathology seen in all of these infectious diseases being explained by activation of the inflammatory system, with the balance between the pro and anti-inflammatory cytokines being tipped towards the onset of systemic inflammation. Although not often expressed in energy terms, there is, when reduced to biochemical essentials, wide agreement that infection with falciparum malaria is often fatal because mitochondria are unable to generate enough ATP to maintain normal cellular function. Most, however, would contend that this largely occurs because sequestered parasitized red cells prevent sufficient oxygen getting to where it is needed. This review considers the evidence that an equally or more important way ATP deficency arises in malaria, as well as these other infectious diseases, is an inability of mitochondria, through the effects of inflammatory cytokines on their function, to utilise available oxygen. This activity of these cytokines, plus their capacity to control the pathways through which oxygen supply to mitochondria are restricted (particularly through directing sequestration and driving anaemia), combine to make falciparum malaria primarily an inflammatory cytokine-driven disease. Article in Journal/Newspaper Arctic Directory of Open Access Journals: DOAJ Articles Arctic Malaria Journal 5 1 |
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Directory of Open Access Journals: DOAJ Articles |
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ftdoajarticles |
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English |
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Arctic medicine. Tropical medicine RC955-962 Infectious and parasitic diseases RC109-216 |
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Arctic medicine. Tropical medicine RC955-962 Infectious and parasitic diseases RC109-216 Alleva Lisa M Budd Alison C Clark Ian A Cowden William B Human malarial disease: a consequence of inflammatory cytokine release |
topic_facet |
Arctic medicine. Tropical medicine RC955-962 Infectious and parasitic diseases RC109-216 |
description |
Abstract Malaria causes an acute systemic human disease that bears many similarities, both clinically and mechanistically, to those caused by bacteria, rickettsia, and viruses. Over the past few decades, a literature has emerged that argues for most of the pathology seen in all of these infectious diseases being explained by activation of the inflammatory system, with the balance between the pro and anti-inflammatory cytokines being tipped towards the onset of systemic inflammation. Although not often expressed in energy terms, there is, when reduced to biochemical essentials, wide agreement that infection with falciparum malaria is often fatal because mitochondria are unable to generate enough ATP to maintain normal cellular function. Most, however, would contend that this largely occurs because sequestered parasitized red cells prevent sufficient oxygen getting to where it is needed. This review considers the evidence that an equally or more important way ATP deficency arises in malaria, as well as these other infectious diseases, is an inability of mitochondria, through the effects of inflammatory cytokines on their function, to utilise available oxygen. This activity of these cytokines, plus their capacity to control the pathways through which oxygen supply to mitochondria are restricted (particularly through directing sequestration and driving anaemia), combine to make falciparum malaria primarily an inflammatory cytokine-driven disease. |
format |
Article in Journal/Newspaper |
author |
Alleva Lisa M Budd Alison C Clark Ian A Cowden William B |
author_facet |
Alleva Lisa M Budd Alison C Clark Ian A Cowden William B |
author_sort |
Alleva Lisa M |
title |
Human malarial disease: a consequence of inflammatory cytokine release |
title_short |
Human malarial disease: a consequence of inflammatory cytokine release |
title_full |
Human malarial disease: a consequence of inflammatory cytokine release |
title_fullStr |
Human malarial disease: a consequence of inflammatory cytokine release |
title_full_unstemmed |
Human malarial disease: a consequence of inflammatory cytokine release |
title_sort |
human malarial disease: a consequence of inflammatory cytokine release |
publisher |
BMC |
publishDate |
2006 |
url |
https://doi.org/10.1186/1475-2875-5-85 https://doaj.org/article/433348442d4b4f0aa435971c1df9ff3a |
geographic |
Arctic |
geographic_facet |
Arctic |
genre |
Arctic |
genre_facet |
Arctic |
op_source |
Malaria Journal, Vol 5, Iss 1, p 85 (2006) |
op_relation |
http://www.malariajournal.com/content/5/1/85 https://doaj.org/toc/1475-2875 doi:10.1186/1475-2875-5-85 1475-2875 https://doaj.org/article/433348442d4b4f0aa435971c1df9ff3a |
op_doi |
https://doi.org/10.1186/1475-2875-5-85 |
container_title |
Malaria Journal |
container_volume |
5 |
container_issue |
1 |
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1766339751100547072 |