ArticleBMC immunology2025
Genetic damage and immune dysregulation in Schistosoma haematobium-infected individuals in Nigeria.
Article in BMC immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundUrogenital schistosomiasis caused by Schistosoma haematobium affects over 100 million people globally, with potential long-term genetic and immunological consequences poorly understood in endemic populations. This study investigates genetic damage and immune dysregulation in infected individuals from a hyperendemic region in Nigeria.
objectiveTo quantify genetic damage markers and characterize immune system alterations in individuals with confirmed S. haematobium infection compared to uninfected controls from Atisbo Local Government Area, Oyo State, Nigeria.
methodsThis cross-sectional study included 240 participants (120 infected, 120 controls) aged 15–65 years, selected using multi-stage cluster sampling. Genetic damage was assessed using comet assay, micronucleus testing, and chromosomal aberration analysis. Immune profiling included Th1/Th2 cytokines, immunoglobulins, and complement components. Multivariate regression models identified independent predictors of genetic damage.
resultsInfected individuals demonstrated markedly elevated genetic damage: comet tail moment 15.7 ± 4.2 versus 6.3 ± 2.1 (Cohen’s d = 2.80, p < 0.001), micronucleus frequency 8.4 ± 2.7 versus 3.1 ± 1.2 per 1000 cells (d = 2.41, p < 0.001), and chromosomal abnormalities 12.3% versus 4.1% (p < 0.001). Pronounced Th2 polarization was evident with IL-4 increased 4.1-fold, IL-5 4.6-fold, and IL-13 4.1-fold, while IFN-γ was reduced by 65% (all p < 0.001, FDR-adjusted). S. haematobium infection independently predicted genetic damage (β = 8.42, 95% CI: 7.51–9.33, p < 0.001) after adjusting for age, BMI, hemoglobin, and sex, explaining 73% of the variance in tail moment values.
conclusionsS. haematobium infection causes substantial genetic damage and Th2-dominant immune dysregulation with potentially serious long-term health consequences. These findings provide scientific justification for intensified control efforts, enhanced post-treatment monitoring, and cancer surveillance programs in endemic populations.
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