Reduced Effective T Helper Responses against Plasmodium falciparum and Schistosoma mansoni Co-Infection in ex vivo: Th1, Th2 & Th17 Immune Responses

Background: Parasitic worms evade immune responses, and interactions between diseases can result in different immunologic outcomes than single infections. These interactions could have an impact on vaccine and chemotherapeutic efficacy. Schistosoma mansoni and Plasmodium falciparum are co-endemic in Uganda and are the most common parasitic causes of public health problems throughout Sub-Saharan Africa. Plasmodium falciparum is the primary cause of malaria, and Schistosoma mansoni is one of the primary causes of intestinal schistosomiasis. Objectives: As a result, the overall goal was, 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. In comparison to the uninfected group, we found an upregulated Th1 T helper subpopulation in independent P. falciparum infections. Independent S. mansoni infections were found to have suboptimal T helper immune responses, with a significantly lower Th1 (Z = 1.425, p = 0.0313) response in comparison to the non-infected group. Suboptimal T helper immune responses were also observed in co-infected individuals, with significantly lower Th1 (Z = 3.260, p = 0.0273) and Th2 (Z = 1.180, p = 0.0078) responses compared to independent P. falciparum infections. S. mansoni infection is a major contributor to a decreased effective T helper immune response.

Author (S) Details

Candia Rowel
Microbiology Department, College of Health Sciences, Makerere University, Kampala, Uganda and Vector Control Division, Ministry of Health, Kampala, Uganda.

Rose Nabatanzi
Microbiology Department, College of Health Sciences, Makerere University, Kampala, Uganda.

Prof. Joseph Olobo
Microbiology Department, College of Health Sciences, Makerere University, Kampala, Uganda.

Ann Auma
Microbiology Department, College of Health Sciences, Makerere University, Kampala, Uganda.

Benon Asiimwe
Microbiology Department, College of Health Sciences, Makerere University, Kampala, Uganda.

Olive Mbabazi
Infectious Diseases Institute, Kampala, Uganda.

Alice Bayiyana
Microbiology Department, College of Health Sciences, Makerere University, Kampala, Uganda.

Annet Enzaru
Vector Control Division, Ministry of Health, Kampala, Uganda.

Edridah Tukahebwa
Vector Control Division, Ministry of Health, Kampala, Uganda.

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