IgM, lgG and IL-6 profiles in the Trypanosoma brucei brucei monkey model of human African trypanosomiasis

Waema, Maxwell W.; Maina, Naomi; Ngotho, Maina; Karanja, Simon; Gachie, Beatrice; Maranga, Dawn Nyawira; Kagira, John

doi:10.1016/j.actatropica.2017.01.012

Cited by 2 publications

(1 citation statement)

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“…It is well documented that HAT is linked to marked alterations in the levels and composition of host lipids and this could be useful in monitoring disease progression [60]. A study by Waema et al [61] reported high cholesterol levels that were constant with the observed hyperlipidemia in a vervet monkey model infected with Trypanosoma brucei rhodesiense. A prior study by Rong et al [59] observed a substantial depletion in the levels of serum lipid profle among mice that were infected with S. mansoni.…”

Section: Discussionmentioning

confidence: 99%

Coinfection with Schistosoma mansoni Enhances Disease Severity in Human African Trypanosomiasis

Mitalo,

Waiganjo,

Mokua Mose

et al. 2023

Journal of Tropical Medicine

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Introduction. Human African trypanosomiasis (HAT) and schistosomiasis are neglected parasitic diseases found in the African continent. This study was conducted to determine how primary infection with Schistosoma mansoni affects HAT disease progression with a secondary infection with Trypanosoma brucei rhodesiense (T.b.r) in a mouse model. Methods. Female BALB-c mice (6–8 weeks old) were randomly divided into four groups of 12 mice each. The different groups were infected with Schistosoma mansoni (100 cercariae) and Trypanosoma brucei rhodesiense (5.0 × 104) separately or together. Twenty-one days after infection with T.b.r, mice were sacrificed and samples were collected for analysis. Results. The primary infection with S. mansoni significantly enhanced successive infection by the T.b.r; consequently, promoting HAT disease severity and curtailing host survival time. T.b.r-induced impairment of the neurological integrity and breach of the blood-brain barrier were markedly pronounced on coinfection with S. mansoni. Coinfection with S. mansoni and T.b.r resulted in microcytic hypochromic anemia characterized by the suppression of RBCs, hematocrit, hemoglobin, and red cell indices. Moreover, coinfection of the mice with the two parasites resulted in leukocytosis which was accompanied by the elevation of basophils, neutrophils, lymphocytes, monocytes, and eosinophils. More importantly, coinfection resulted in a significant elevation of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bilirubin, creatinine, urea, and uric acid, which are the markers of liver and kidney damage. Meanwhile, S. mansoni-driven dyslipidemia was significantly enhanced by the coinfection of mice with T.b.r. Moreover, coinfection with S. mansoni and T.b.r led to a strong immune response characterized by a significant increase in serum TNF-α and IFN-γ. T.b.r infection enhanced S. mansoni-induced depletion of cellular-reduced glutathione (GSH) in the brain and liver tissues, indicative of lethal oxidative damage. Similarly, coinfection resulted in a significant rise in nitric oxide (NO) and malondialdehyde (MDA) levels. Conclusion. Primary infection with S. mansoni exacerbates disease severity of secondary infection with T.b.r in a mouse model that is associated with harmful inflammatory response, oxidative stress, and organ injury.

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Section: Discussionmentioning

confidence: 99%