Co-infection with Trypanosoma cruzi protects mice against early death by neurological or pulmonary disorders induced by Plasmodium berghei ANKA

Abstract

Objective: The objective of this study was to investigate whether the infection of C57BL/6 mice by P. berghei ANKA, which causes severe malaria, was modulated by co-infection with Trypanosoma cruzi. Methods:Groups of C57BL/6 mice were infected either with P. berghei ANKA, T. cruzi strain G, or with both parasites. The presence of parasites was checked by microscopic examination of blood samples. Symptoms of neurological or respiratory disorders, as well as mortality, were registered. Breakdown of the blood brain barrier was determined by injecting the dye Evans blue. Histological sections of the lung were prepared and stained with hematoxilin-eosin.Results: All mice infected only with P. berghei ANKA died within 7-11 days post-infection, either with symptoms of cerebral malaria or with respiratory abnormalities. The animals co-infected with T. cruzi strain G survived longer, without any of the referred to symptoms. Protection against the early death by severe malaria was effective when mice were given T. cruzi 15 days before P. berghei inoculation. Breakdown of the blood brain barrier and extensive pulmonary oedema, caused by malaria parasites, were much less pronounced in co-infected mice. The degree of protection to severe malaria and early death, conferred by co-infection with T. cruzi, was comparable to that conferred by treatment with anti-CD8 antibodies. Conclusion:Co-infection with T. cruzi protects C57BL/6 against the early death by malaria infection, by partially preventing either the breakdown of the blood brain, and cerebral malaria as a consequence, or the pulmonary oedema.

Disruption of the blood–brain barrier in pigs naturally infected with Taenia solium, untreated and after anthelmintic treatment

“…It is also well documented that the complex formed by EB and albumin is excluded from the brain parenchyma by a fully functional BBB, so brain tissue from uninfected controls would have remained unstained by EB (Okamura et al, 2010; Marchi et al, 2010). This has been a consistent observation in a number of studies in which EB was used to evaluate the integrity of the BBB in experimental settings, such as Plasmodium infections in mice (Egima et al, 2007) and ultrasound-induced vascular disruption in rats (Wei et al, 2013). In the case of NCC, involvement of the BBB has been reported in the murine model by demonstrating migration of leukocytes in the brain of mice experimentally infected with Mesocestoides corti (Alvarez and Teale, 2006).…”

Maladjusted Host Immune Responses Induce Experimental Cerebral Malaria-Like Pathology in a Murine Borrelia and Plasmodium Co-Infection Model

“…It decreases the risk of severe malaria disease albeit increases the chances for clinical malaria early in the infection. A similar phenomenon was observed in murine co-infections with Trypanosoma cruz i and P. berghei ANKA, where the acute symptoms and pathological signs of ECM were absent [55] . There is a lack of data regarding Plasmodium and acute bacterial infection pathology.…”

Trypanosoma brucei infection protects mice against malaria

“…Several studies have demonstrated that the course of a Plasmodium infection can be influenced by the presence of a second pathogen in the same host, either by aggravating malaria-associated pathology [21, 42], or by conferring protection against disease severity [43, 44]. However, despite the geographical overlap between the etiological agents of sleeping sickness and malaria, whether an ongoing infection by T .…”

“…cruzi and P . berghei do not develop ECM symptoms, presumably due to a reduction in the accumulation of CD8 + T cells in the brain of those animals [44]. Therefore, during a T .…”