Abstract
Background: Parasitic worms evade immune responses, and interactions between diseases can cause altered immunologic outcomes compared to what usually occurs with single infections. These interactions may influence vaccine and chemotherapeutic efficacy. Schistosoma mansoni and Plasmodium falciparum are co-endemic in Uganda and are the leading parasitic causes of public health problems across sub-Saharan Africa. Objectives: The overall aim was therefore, to elucidate the impact of S. mansoni infection on protective T helper immune responses on P. falciparum and S. mansoni co-infection. Methodology: This study evaluated the T helper immune responses in individuals with independent S. mansoni infection, independent P. falciparum infection, co-infection and non-infection in school attending children in a co-endemic area along Lake Victoria shores, Uganda. Immune responses were categorized into Th1, Th2, and Th17 based on unique cytokine(s) produced by the T helper subpopulation in ex vivo. Kato Katz thick smears and circulating cathodic antigen tests were performed for S. mansoni screening, whereas thick and thin blood smear techniques were performed for P. falciparum screening. Results: We observed an up regulated Th1 T helper subpopulation in independent P. falciparum infections compared to the uninfected group. Suboptimal T helper immune responses were detected in independent S. mansoni infections characterized by significantly down regulated Th1 (Z = -1.425, p = 0.0313) response in comparison to the non-infected group. Suboptimal T helper immune responses were also recorded in the co-infected individuals characterized by significantly down regulated Th1 (Z = -3.260, p = 0.0273) and Th2 (Z = -1.180, p = 0.0078) responses compared to independent P. falciparum. Conclusions: S. mansoni infection is a major contributor of a reduced effective T helper immune response against P. falciparum in P. falciparum and S. mansoni co-infection.
Highlights
Schistosoma mansoni is one of the causative agents of intestinal schistosomiasis and Plasmodium falciparum is the major causative agent of malaria
Suboptimal T helper immune responses were recorded in the co-infected individuals characterized by significantly down regulated Th1 (Z = −3.260, p = 0.0273) and Th2 (Z = −1.180, p = 0.0078) responses compared to independent P. falciparum
Of the 40 participants included for ex vivo T helper phenotyping from their Peripheral Blood Mononuclear Cells (PBMCs), there was a significant difference in the burden of S. mansoni infection between the co-infected group compared to S. mansoni only infections (F(11, 11) = 7.898, p = 0.0019)
Summary
Schistosoma mansoni is one of the causative agents of intestinal schistosomiasis and Plasmodium falciparum is the major causative agent of malaria. Parasitic worms evade immune responses [7]-[14] and interactions between diseases can cause altered immunologic outcomes compared to what usually occurs with single infections [15] These differential outcomes may influence vaccine and chemotherapeutic efficacy [16] [17]. The overall aim was to elucidate the impact of S. mansoni infection on protective T helper immune responses in P. falciparum and S. mansoni co-infection This will help provide evidence to evaluate chemotherapy and vaccine efficacy to these diseases especially in co-infection situations. Parasitic worms evade immune responses, and interactions between diseases can cause altered immunologic outcomes compared to what usually occurs with single infections These interactions may influence vaccine and chemotherapeutic efficacy. Conclusions: S. mansoni infection is a major contributor of a reduced effective T helper immune response against P. falciparum in P. falciparum and S. mansoni co-infection
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