Trypanosoma brucei infection protects mice against malaria.

Sleeping sickness and malaria are parasitic diseases with overlapping geographical distributions in sub-Saharan Africa. We hypothesized that the immune response elicited by an infection with Trypanosoma brucei, the etiological agent of sleeping sickness, would inhibit a subsequent infection by Plasm...

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Main Authors: Margarida Sanches-Vaz, Adriana Temporão, Rafael Luis, Helena Nunes-Cabaço, António M Mendes, Sarah Goellner, Tânia Carvalho, Luisa M Figueiredo, Miguel Prudêncio
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2019-11-01
Series:PLoS Pathogens
Online Access:https://doi.org/10.1371/journal.ppat.1008145
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spelling doaj-11bc7f2ce60040e9806d86a0039cea292021-04-21T17:09:12ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742019-11-011511e100814510.1371/journal.ppat.1008145Trypanosoma brucei infection protects mice against malaria.Margarida Sanches-VazAdriana TemporãoRafael LuisHelena Nunes-CabaçoAntónio M MendesSarah GoellnerTânia CarvalhoLuisa M FigueiredoMiguel PrudêncioSleeping sickness and malaria are parasitic diseases with overlapping geographical distributions in sub-Saharan Africa. We hypothesized that the immune response elicited by an infection with Trypanosoma brucei, the etiological agent of sleeping sickness, would inhibit a subsequent infection by Plasmodium, the malaria parasite, decreasing the severity of its associated pathology. To investigate this, we established a new co-infection model in which mice were initially infected with T. brucei, followed by administration of P. berghei sporozoites. We observed that a primary infection by T. brucei significantly attenuates a subsequent infection by the malaria parasite, protecting mice from experimental cerebral malaria and prolonging host survival. We further observed that an ongoing T. brucei infection leads to an accumulation of lymphocyte-derived IFN-γ in the liver, limiting the establishment of a subsequent hepatic infection by P. berghei sporozoites. Thus, we identified a novel host-mediated interaction between two parasitic infections, which may be epidemiologically relevant in regions of Trypanosoma/Plasmodium co-endemicity.https://doi.org/10.1371/journal.ppat.1008145
collection DOAJ
language English
format Article
sources DOAJ
author Margarida Sanches-Vaz
Adriana Temporão
Rafael Luis
Helena Nunes-Cabaço
António M Mendes
Sarah Goellner
Tânia Carvalho
Luisa M Figueiredo
Miguel Prudêncio
spellingShingle Margarida Sanches-Vaz
Adriana Temporão
Rafael Luis
Helena Nunes-Cabaço
António M Mendes
Sarah Goellner
Tânia Carvalho
Luisa M Figueiredo
Miguel Prudêncio
Trypanosoma brucei infection protects mice against malaria.
PLoS Pathogens
author_facet Margarida Sanches-Vaz
Adriana Temporão
Rafael Luis
Helena Nunes-Cabaço
António M Mendes
Sarah Goellner
Tânia Carvalho
Luisa M Figueiredo
Miguel Prudêncio
author_sort Margarida Sanches-Vaz
title Trypanosoma brucei infection protects mice against malaria.
title_short Trypanosoma brucei infection protects mice against malaria.
title_full Trypanosoma brucei infection protects mice against malaria.
title_fullStr Trypanosoma brucei infection protects mice against malaria.
title_full_unstemmed Trypanosoma brucei infection protects mice against malaria.
title_sort trypanosoma brucei infection protects mice against malaria.
publisher Public Library of Science (PLoS)
series PLoS Pathogens
issn 1553-7366
1553-7374
publishDate 2019-11-01
description Sleeping sickness and malaria are parasitic diseases with overlapping geographical distributions in sub-Saharan Africa. We hypothesized that the immune response elicited by an infection with Trypanosoma brucei, the etiological agent of sleeping sickness, would inhibit a subsequent infection by Plasmodium, the malaria parasite, decreasing the severity of its associated pathology. To investigate this, we established a new co-infection model in which mice were initially infected with T. brucei, followed by administration of P. berghei sporozoites. We observed that a primary infection by T. brucei significantly attenuates a subsequent infection by the malaria parasite, protecting mice from experimental cerebral malaria and prolonging host survival. We further observed that an ongoing T. brucei infection leads to an accumulation of lymphocyte-derived IFN-γ in the liver, limiting the establishment of a subsequent hepatic infection by P. berghei sporozoites. Thus, we identified a novel host-mediated interaction between two parasitic infections, which may be epidemiologically relevant in regions of Trypanosoma/Plasmodium co-endemicity.
url https://doi.org/10.1371/journal.ppat.1008145
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