Trypanosoma brucei infection protects mice against malaria

Sanches-Vaz, Margarida; Temporão, Adriana; Luís, Rafael; Nunes‐Cabaço, Helena; Mendes, António M.; Goellner, Sarah; Carvalho, Tânia; Figueiredo, Luísa M.; Prudêncio, Miguel

doi:10.1371/journal.ppat.1008145

Cited by 12 publications

(25 citation statements)

References 78 publications

(82 reference statements)

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“…These results indicate, however, that Anopheles mosquitoes could be exposed to Trypanosoma parasites when they feed on infected animals. Thus, as observed by Sanches-Vaz and others [12] in mice, this can conduct to a reduction of infection in Anopheles mosquitoes. Indeed, the absence of plasmodial infection in the sites where animals were found infected with T. vivax (sites with low malaria prevalence) and the presence of plasmodial infections in sites without trypanosome-infected animals, would be in favour of the involvement of trypanosomal infection in the plasmodial infection.…”

Section: Discussionsupporting

confidence: 62%

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Possible influence of Plasmodium/Trypanosoma co-infections on the vectorial capacity of Anopheles mosquitoes

et al. 2020

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Objective: In tropical Africa, trypanosomiasis is present in endemic areas with many other diseases including malaria. Because malaria vectors become more anthropo-zoophilic under the current insecticide pressure, they may be exposed to trypanosome parasites. By collecting mosquitoes in six study sites with distinct malaria infection prevalence and blood sample from cattle, we tried to assess the influence of malaria-trypanosomiasis co-endemicity on the vectorial capacity of Anopheles. Results: Overall, all animal infections were due to Trypanosoma vivax (infection rates from 2.6 to 10.5%) in villages where the lowest Plasmodium prevalence were observed at the beginning of the study. An. gambiae s.l. displayed trophic preferences for human-animal hosts. Over 84 mosquitoes, only one was infected by Plasmodium falciparum (infection rate: 4.5%) in a site that displayed the highest prevalence at the beginning of the study. Thus, Anopheles could be exposed to Trypanosoma when they feed on infected animals. No Plasmodium infection was observed in the Trypanosoma-infected animals sites. This can be due to an interaction between both parasites as observed in mice and highlights the need of further studies considering Trypanosoma/Plasmodium mixed infections to better characterize the role of these infections in the dynamic of malaria transmission and the mechanisms involved.

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Section: Discussionsupporting

confidence: 62%

“…In a recent study, Sanches-Vaz and others [12] showed through a co-infection model, that mice primarily infected with T. brucei, followed by the administration of P. berghei sporozoites, are protected from experimental cerebral malaria and presented increased host survival. In addition, subsequent infection of An.…”

Section: Introductionmentioning

confidence: 99%

Possible influence of Plasmodium/Trypanosoma co-infections on the vectorial capacity of Anopheles mosquitoes

et al. 2020

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“…brucei strongly impairs a secondary infection by P . berghei sporozoites in mice [ 27 ], similarly to what has been previously shown for the co-infection between Schistosoma and Plasmodium [ 28 ].…”

Section: Introductionsupporting

confidence: 62%

Excreted Trypanosoma brucei proteins inhibit Plasmodium hepatic infection

et al. 2021

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Malaria, a disease caused by Plasmodium parasites, remains a major threat to public health globally. It is the most common disease in patients with sleeping sickness, another parasitic illness, caused by Trypanosoma brucei. We have previously shown that a T. brucei infection impairs a secondary P. berghei liver infection and decreases malaria severity in mice. However, whether this effect requires an active trypanosome infection remained unknown. Here, we show that Plasmodium liver infection can also be inhibited by the serum of a mouse previously infected by T. brucei and by total protein lysates of this kinetoplastid. Biochemical characterisation showed that the anti-Plasmodium activity of the total T. brucei lysates depends on its protein fraction, but is independent of the abundant variant surface glycoprotein. Finally, we found that the protein(s) responsible for the inhibition of Plasmodium infection is/are present within a fraction of ~350 proteins that are excreted to the bloodstream of the host. We conclude that the defence mechanism developed by trypanosomes against Plasmodium relies on protein excretion. This study opens the door to the identification of novel antiplasmodial intervention strategies.

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“…Experimental visceral leishmaniasis (VL) was also shown to confer enhanced protection against Streptococcus pneumoniae sepsis 6 . Similarly, in experimental models of malaria as a concurrent or superimposed infection, aggravating or protective responses were noticed 7 – 10 , suggestive of the role of immune dysregulation.…”

Section: Introductionmentioning

confidence: 92%

Hematological consequences of malaria in mice previously treated for visceral leishmaniasis

et al. 2021

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Background: Polyparasitism is commonplace in countries where endemicity for multiple parasites exists, and studies in animal models of coinfection have made significant inroads into understanding the impact of often competing demands on the immune system. However, few studies have addressed how previous exposure to and treatment for one infection impacts a subsequent heterologous infection. Methods: We used a C57BL/6 mouse model of drug-treated Leishmania donovani infection followed by experimental Plasmodium chabaudi AS malaria, focusing on hematological dysfunction as a common attribute of both infections. We measured parasite burden, blood parameters associated with anemia and thrombocytopenia, and serum thrombopoietin. In addition, we quantified macrophage iNOS expression through immunohistological analysis of the liver and spleen. Results: We found that the thrombocytopenia and anemia that accompanies primary L. donovani infection was rapidly reversed following single dose AmBisome® treatment, along with multiple other markers associated with immune activation (including restoration of tissue microarchitecture and reduced macrophage iNOS expression). Compared to naive mice, mice cured of previous L. donovani infection showed comparable albeit delayed clinical responses (including peak parasitemia and anemia) to P. chabaudi AS infection. Thrombocytopenia was also evident in these sequentially infected mice, consistent with a decrease in circulating levels of thrombopoietin. Architectural changes to the spleen were also comparable in sequentially infected mice compared to those with Plasmodium infection alone. Conclusions: Our data suggest that in this sequential infection model, previously-treated L. donovani infection has limited impact on the subsequent development of Plasmodium infection, but this issue deserves further attention in models of more severe disease or through longitudinal population studies in humans.

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Trypanosoma brucei infection protects mice against malaria

Cited by 12 publications

References 78 publications

Possible influence of Plasmodium/Trypanosoma co-infections on the vectorial capacity of Anopheles mosquitoes

Possible influence of Plasmodium/Trypanosoma co-infections on the vectorial capacity of Anopheles mosquitoes

Excreted Trypanosoma brucei proteins inhibit Plasmodium hepatic infection

Hematological consequences of malaria in mice previously treated for visceral leishmaniasis

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