TY - JOUR
T1 - Trypanosoma brucei infection protects mice against malaria
AU - Sanches-Vaz, Margarida
AU - Temporão, Adriana
AU - Luis, Rafael
AU - Nunes-Cabaço, Helena
AU - Mendes, António M.
AU - Goellner, Sarah
AU - Carvalho, Tania
AU - Figueiredo, Luisa M.
AU - PrudêncioI, Miguel
N1 - Funding Information:
Funding:ThisstudywassupportedbyFundac ¸ão paraaCiênciaeTecnologia,Portugal(FCT)grants UID/BIM/50005/2019(Ministe ´ riodaCiência, TecnologiaeEnsinoSuperior(MCTES)through FundosdoOrc ¸amentodeEstado)andPTDC-SAU-INF-29550-2017toM.P.M.S.-V.wassupportedby aFCTfellowshipPD/BD/105838/2014.A.T.was supportedbyaFCTfellowshipPD/BD/138891/
Publisher Copyright:
© 2019 Sanches-Vaz et al.
PY - 2019
Y1 - 2019
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85075813707&partnerID=8YFLogxK
UR - http://10.1371/journal.ppat.1008145
U2 - 10.1371/journal.ppat.1008145
DO - 10.1371/journal.ppat.1008145
M3 - Article
C2 - 31703103
AN - SCOPUS:85075813707
SN - 1553-7366
VL - 15
JO - PLoS Pathogens
JF - PLoS Pathogens
IS - 11
M1 - e1008145
ER -