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Tumour necrosis factor-α and macrophages in Plasmodium berghei-induced cerebral malaria

Published online by Cambridge University Press:  06 April 2009

J. H. A. J. Curfs ,
C. C. Hermsen ,
P. Kremsner ,
S. Neifer ,
J. H. E. Th. Meuwissen ,
N. Van Rooyen  and
W. M. C. Eling
J. H. A. J. Curfs
Affiliation:
Department of Medical Microbiology, Catholic University of Nijmegen, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands
C. C. Hermsen
Affiliation:
Department of Medical Microbiology, Catholic University of Nijmegen, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands
P. Kremsner
Affiliation:
Landesinstitut für Tropenmedizin, Berlin, Germany
S. Neifer
Affiliation:
Landesinstitut für Tropenmedizin, Berlin, Germany
J. H. E. Th. Meuwissen
Affiliation:
Department of Medical Microbiology, Catholic University of Nijmegen, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands
N. Van Rooyen
Affiliation:
Department of Histology, Free University, Amsterdam
W. M. C. Eling
Affiliation:
Department of Medical Microbiology, Catholic University of Nijmegen, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands
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Summary

The effect of tumour necrosis factor-α on malaria-infected mice was studied. C57B1/6J mice infected with Plasmodium berghei K173 exhibited an increased sensitivity to exogenous TNF. Injection of 15 μg TNF was lethal to some of the animals when given 5–7 days after infection, while when given later on in the infection (i.e. days 8–10) amounts as low as 2·5 μg TNF appeared to be lethal in all mice. The pathology in infected mice treated with TNF resembled that found in the brains of infected mice dying with cerebral malaria. Infected mice treated with TNF, however, also developed severe pathological changes in other organs. On the contrary, treatment with sublethal amounts of TNF (1·0 μg or less) given on days 8 and 9 after infection, protected mice against the development of cerebral malaria. In addition, infected mice exhibited an enhanced sensitivity for treatment with lipopolysaccharide (LPS). Sublethal amounts of LPS, however, did not prevent mortality as in TNF-treated mice (LPS-treated mice died at about the same time as infected mice that developed cerebral malaria), but no cerebral haemorrhages were found in the majority of LPS treated, infected animals. Treatment with dexamethasone during infection protected mice against the development of cerebral malaria, but did not suppress their increased sensitivity to exogenous TNF. Treatment of mice with liposome-encapsulated dichloromethylene diphosphonate (lip-Cl2MDP), used to eliminate macrophages (an important source of TNF), prevented the development of cerebral malaria, but only when given before day 5 of infection. Mice protected by treatment with lip Cl2MDP, however, remained sensitive for LPS on the eighth day of infection.

Keywords

cerebral malariaPlasmodium bergheiTNFmacrophages
Type
Research Article
Information
Parasitology , Volume 107 , Issue 2 , August 1993 , pp. 125 - 134
Copyright
Copyright © Cambridge University Press 1993

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