Plasmodium knowlesi H strain pregnancy malaria immune responses in olive baboons (Papio anubis)

TL;DR

This study uses baboons infected with Plasmodium knowlesi to investigate immune responses during pregnancy malaria, revealing cytokine response patterns similar to humans, which supports their use as a model for this disease.

Contribution

It demonstrates that baboons can serve as a relevant model for studying immune mechanisms in pregnancy malaria, highlighting cytokine response alterations during infection.

Findings

Pregnancy malaria in baboons suppresses interferon gamma and IL-6 responses.

Tumour necrosis factor alpha is upregulated during infection.

The immune response patterns are similar to those observed in humans.

Abstract

Approximately 24 million pregnant women in Sub-Saharan Africa are at risk of suffering from pregnancy malaria complications. Mechanisms responsible for increased susceptibility to malaria in pregnant women are not fully understood. Baboons are susceptible to Plasmodium knowlesi and their reproductive physiology and host pathogen interactions are similar to those in humans, making them attractive for development as a model for studying mechanisms underlying pregnancy malaria. This study exploited the susceptibility of baboons to Plasmodium knowlesi infection to characterize cytokine and peripheral blood mononuclear cell recall proliferation responses underlying the pathogenesis of pregnancy malaria in baboons infected with Plasmodium knowlesi. The pregnancies of three time mated adult female baboons and their gestational levels were confirmed by ultrasonography. On the 150th day of gestation, the pregnant baboons together with four non pregnant controls were infected with Plasmodium knowlesi H strain parasites. Collection of peripheral sera, and mononuclear cells was then done on a weekly basis. Sera cytokine concentrations were measured by Enzyme Linked Immunosorbent Assay (ELISA) using respective enzyme conjugated antibodies. Peripheral blood mononuclear cell recall proliferation assays were also done on a weekly basis. Results indicate that pregnancy malaria in this model is associated with suppression of interferon gamma and interleukin 6 (IL-6) responses. Tumour necrosis factor alpha responses were upregulated while IL-4, IL-12 and recall proliferation responses were not different from controls. These data to a great extent are consistent with some findings from human studies, showing the feasibility of this model for studying mechanisms underlying pregnancy malaria.