Chronic S. Mansoni Infection Critically Regulates PbA Infection-associated Severity and Pathological Events in a Mouse Model

Abstract

The parasite Plasmodium is responsible for the severe infection known as malaria. The infection causes high mortality and morbidity, especially in endemic areas worldwide. Schistosomes which are blood flukes are the primary cause of schistosomiasis, which is the second most common parasitic illness in terms of morbidity and death after malaria. In many areas, both of these illnesses are co-endemic. Biochemically, each parasite utilizes the host protein differently and has defined immunological and physiological responses. This study sought to assess how persistent S. mansoni infection affected the severity of the P. berghei ANKA-associated illness and other pathological events in a mouse model during co-infection. Mice were infected with 200 Schistosoma mansoni cercaria. After chronic S. mansoni infection had been established, mice in the coinfection group were inoculated with 10,000 PbA-infected red blood cells. Physiological parameters were monitored at a two-day interval, to track the infection levels. Furthermore, liver andkidney function tests and oxidative stress markers were quantified at the end of the study and analyzed at a p < 0.05. Co-infection of S. mansoni and PbA enhanced the survival of mice whichwas independent of parasitemia preventing lethal experimental malaria in the majority of mice and prevented hepatosplenomegaly. Chronic S. mansoni infection resulted in hepatosplenomegaly which contributed to an increase in body weight while the introduction of malaria in the host reduced body weight. Liver functionality was disrupted by the measurement of the ALP enzyme, a marker of liver damage. Schistosomiasis reduced host metabolites such as protein, and lipids as schistosomes cannot synthesize their own de novo. Co-infection restored the disruptive effect of S. mansoni in the host. There was evident oxidative stress in the host, liver, and brain of mice infected with S. mansoni or PbA alone. However, coinfection of S. mansoni and PbA ameliorated oxidative stress with concomitant attenuation of organ injury hence reinforcing protection observed in experimental malaria. Overall, this study demonstrates that chronic S. mansoni infection is critical in the regulation of PbA infection-associated severity & pathological events in a mouse model.