Murine cerebral malaria: The whole story

Hunt, Nicholas H., Grau, Georges E., Engwerda, Christian, Barnum, Scott R., van der Heyde, Henri, Hansen, Diana S., Schofield, Louis and Golenser, Jacob (2010) Murine cerebral malaria: The whole story. Trends in Parasitology, 26 6: 272-274. doi:10.1016/j.pt.2010.03.006

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Author Hunt, Nicholas H.
Grau, Georges E.
Engwerda, Christian
Barnum, Scott R.
van der Heyde, Henri
Hansen, Diana S.
Schofield, Louis
Golenser, Jacob
Title Murine cerebral malaria: The whole story
Journal name Trends in Parasitology   Check publisher's open access policy
ISSN 1471-4922
1471-5007
0169-4758
Publication date 2010-06
Sub-type Letter to editor, brief commentary or brief communication
DOI 10.1016/j.pt.2010.03.006
Volume 26
Issue 6
Start page 272
End page 274
Total pages 3
Editor R. Lynn Sherrer
Place of publication London, U.K.
Publisher Elsevier
Collection year 2011
Language eng
Formatted abstract
In the Opinion of White and colleagues, ‘The value of the mouse model in identifying pathological processes or therapeutic interventions in human cerebral malaria is questionable.’ Surprisingly, this conclusion was presented without discussion of any of the numerous similarities between the cerebral syndromes caused by Plasmodium falciparum in humans and the P. berghei ANKA strain in mice that have been described in several detailed reviews.

In their article, White et al. claimed that, ‘There are now more than ten times as many studies each year of the murine model than on human cerebral malaria’. To generate the data presented in Figure 1 of their article, their literature search for studies involving human cerebral malaria (HCM) was constrained (‘limits, concerning therapy, clinical trials’) whereas that for murine cerebral malaria (MCM) was not. Thus the basic scientific principle of drawing conclusions from comparable data was not applied.

We agree wholeheartedly with White and colleagues that there is a need for more pathological studies of severe falciparum malaria and would welcome any opportunity for further involvement in such studies. We suggest that they might include investigation of the possible roles of γ-interferon, lymphotoxin α, chemokines, perforin and innate immunity in the pathogenesis of HCM, as well as the mechanisms of endothelial activation and glial changes.
© 2010 Elsevier Ltd. All rights reserved.
Keyword Gene-expression
Brain
Encephalomyelitis
Pathogenesis
Q-Index Code CX
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Letter to editor, brief commentary or brief communication
Collections: Non HERDC
School of Medicine Publications
 
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Created: Mon, 28 Mar 2011, 09:59:35 EST by Lisa Hennell on behalf of !NON-HERDC