Cerebral malaria protection in mice by species-specific Plasmodium coinfection is associated with reduced CC chemokine levels in the brain

Clark, C.J. and Phillips, R.S. (2011) Cerebral malaria protection in mice by species-specific Plasmodium coinfection is associated with reduced CC chemokine levels in the brain. Parasite Immunology, 33(11), pp. 637-641. (doi: 10.1111/j.1365-3024.2011.01329.x)

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Abstract

Cerebral malaria is a major pathological complication of Plasmodium falciparum infection in humans. Epidemiological observations have suggested that the clinical evolution of P. falciparum infections may be influenced by the concurrent presence of another Plasmodium species. Infection of susceptible mouse strains with P. berghei ANKA (PbA) provides an experimental model of cerebral malaria which has been extensively used to identify different components of the immune system involved in cerebral malaria. This model has also been employed to investigate the influence of experimental mixed-Plasmodium-species infections on the expression of cerebral malaria; PbA-induced cerebral malaria is completely inhibited by the simultaneous presence of P. yoelii yoelii 17X clone 1.1 parasites, and accumulation of CD8(+) T cells in the brain vasculature is abolished. We investigated whether brain levels of CD8(+) -T-cell-chemoattractant chemokines CCL3, CCL4, and CCL5 are reduced in these protected coinfected mice compared with PbA-infected mice. Coinfected mice were found to exhibit significantly reduced levels of all three chemokines on day 6 post-infection. This finding may contribute to the abolition of the accumulation of CD8(+) T cells in the brain vasculature and the prevention of the development of cerebral malaria in coinfected mice.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Phillips, Professor Stephen
Authors: Clark, C.J., and Phillips, R.S.
College/School:College of Medical Veterinary and Life Sciences > School of Life Sciences
Journal Name:Parasite Immunology
Publisher:Wiley-Blackwell Publishing Ltd.
ISSN:0141-9838
ISSN (Online):1365-3024

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