Schistosoma co-infection protects against brain pathology but does not prevent severe disease and death in a murine model of cerebral malaria.

2.50
Hdl Handle:
http://hdl.handle.net/10033/123486
Title:
Schistosoma co-infection protects against brain pathology but does not prevent severe disease and death in a murine model of cerebral malaria.
Authors:
Bucher, Kirsten; Dietz, Klaus; Lackner, Peter; Pasche, Bastian; Fendel, Rolf; Mordmüller, Benjamin; Ben-Smith, Anne; Hoffmann, Wolfgang H
Abstract:
Co-infections of helminths and malaria parasites are common in human populations in most endemic areas. It has been suggested that concomitant helminth infections inhibit the control of malaria parasitemia but down-modulate severe malarial disease. We tested this hypothesis using a murine co-infection model of schistosomiasis and cerebral malaria. C57BL/6 mice were infected with Schistosoma mansoni and 8-9 weeks later, when Schistosoma infection was patent, mice were co-infected with Plasmodium berghei ANKA strain. We found that a concomitant Schistosoma infection increased parasitemia at the beginning of the P. berghei infection. It did not protect against P. berghei-induced weight loss and hypothermia, and P. berghei-mono-infected as well as S. mansoni-P. berghei-co-infected animals showed a high case fatality between days 6 and 8 of malarial infection. However, co-infection significantly reduced P. berghei-induced brain pathology. Over 40% of the S. mansoni-P. berghei-co-infected animals that died during this period were completely protected against haemorrhaging, plugging of blood vessels and infiltration, indicating that mortality in these animals was not related to cerebral disease. Schistosoma mansoni-P. berghei-co-infected mice had elevated plasma concentrations of IL-5 and IL-13 and on day 6 lower levels of IFN-γ, IL-10, monocyte chemoattractant protein-1 (MCP-1) and monokine induced by IFN-γ (MIG) than P. berghei-mono-infected mice. We conclude that in P. berghei infections, disease and early death are caused by distinct pathogenic mechanisms, which develop in parallel and are differentially influenced by the immune response to S. mansoni. This might explain why, in co-infected mice, death could be induced in the absence of brain pathology.
Affiliation:
Institute of Tropical Medicine, University of Tübingen, Tübingen, Germany.
Citation:
Schistosoma co-infection protects against brain pathology but does not prevent severe disease and death in a murine model of cerebral malaria. 2011, 41 (1):21-31 Int. J. Parasitol.
Journal:
International journal for parasitology
Issue Date:
Jan-2011
URI:
http://hdl.handle.net/10033/123486
DOI:
10.1016/j.ijpara.2010.06.008
PubMed ID:
20708623
Type:
Article
Language:
en
ISSN:
1879-0135
Appears in Collections:
publications of the department infection genetics (INFG)

Full metadata record

DC FieldValue Language
dc.contributor.authorBucher, Kirstenen
dc.contributor.authorDietz, Klausen
dc.contributor.authorLackner, Peteren
dc.contributor.authorPasche, Bastianen
dc.contributor.authorFendel, Rolfen
dc.contributor.authorMordmüller, Benjaminen
dc.contributor.authorBen-Smith, Anneen
dc.contributor.authorHoffmann, Wolfgang Hen
dc.date.accessioned2011-03-03T15:22:40Z-
dc.date.available2011-03-03T15:22:40Z-
dc.date.issued2011-01-
dc.identifier.citationSchistosoma co-infection protects against brain pathology but does not prevent severe disease and death in a murine model of cerebral malaria. 2011, 41 (1):21-31 Int. J. Parasitol.en
dc.identifier.issn1879-0135-
dc.identifier.pmid20708623-
dc.identifier.doi10.1016/j.ijpara.2010.06.008-
dc.identifier.urihttp://hdl.handle.net/10033/123486-
dc.description.abstractCo-infections of helminths and malaria parasites are common in human populations in most endemic areas. It has been suggested that concomitant helminth infections inhibit the control of malaria parasitemia but down-modulate severe malarial disease. We tested this hypothesis using a murine co-infection model of schistosomiasis and cerebral malaria. C57BL/6 mice were infected with Schistosoma mansoni and 8-9 weeks later, when Schistosoma infection was patent, mice were co-infected with Plasmodium berghei ANKA strain. We found that a concomitant Schistosoma infection increased parasitemia at the beginning of the P. berghei infection. It did not protect against P. berghei-induced weight loss and hypothermia, and P. berghei-mono-infected as well as S. mansoni-P. berghei-co-infected animals showed a high case fatality between days 6 and 8 of malarial infection. However, co-infection significantly reduced P. berghei-induced brain pathology. Over 40% of the S. mansoni-P. berghei-co-infected animals that died during this period were completely protected against haemorrhaging, plugging of blood vessels and infiltration, indicating that mortality in these animals was not related to cerebral disease. Schistosoma mansoni-P. berghei-co-infected mice had elevated plasma concentrations of IL-5 and IL-13 and on day 6 lower levels of IFN-γ, IL-10, monocyte chemoattractant protein-1 (MCP-1) and monokine induced by IFN-γ (MIG) than P. berghei-mono-infected mice. We conclude that in P. berghei infections, disease and early death are caused by distinct pathogenic mechanisms, which develop in parallel and are differentially influenced by the immune response to S. mansoni. This might explain why, in co-infected mice, death could be induced in the absence of brain pathology.en
dc.language.isoenen
dc.titleSchistosoma co-infection protects against brain pathology but does not prevent severe disease and death in a murine model of cerebral malaria.en
dc.typeArticleen
dc.contributor.departmentInstitute of Tropical Medicine, University of Tübingen, Tübingen, Germany.en
dc.identifier.journalInternational journal for parasitologyen

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