Olaniyan Mathew Folaranmi, Odegbemi Odekunle Bola, Iyare Godfrey Innocent, Alaka Olubunmi Olayemi, Adepoju Ademola Lukman
Department of Medical Laboratory Science, Edo State University, Uzairue, Edo State, Nigeria.
Department of Medical Laboratory Science, Nigerian Navy Hospital, Warri, Delta State, Nigeria.
BMC Immunol. 2025 Sep 2;26(1):65. doi: 10.1186/s12865-025-00749-w.
Urogenital schistosomiasis caused by 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.
To quantify genetic damage markers and characterize immune system alterations in individuals with confirmed infection compared to uninfected controls from Atisbo Local Government Area, Oyo State, Nigeria.
This 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.
Infected individuals demonstrated markedly elevated genetic damage: comet tail moment 15.7 ± 4.2 versus 6.3 ± 2.1 (Cohen’s d = 2.80, < 0.001), micronucleus frequency 8.4 ± 2.7 versus 3.1 ± 1.2 per 1000 cells (d = 2.41, < 0.001), and chromosomal abnormalities 12.3% versus 4.1% ( < 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 < 0.001, FDR-adjusted). infection independently predicted genetic damage (β = 8.42, 95% CI: 7.51–9.33, < 0.001) after adjusting for age, BMI, hemoglobin, and sex, explaining 73% of the variance in tail moment values.
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.
The online version contains supplementary material available at 10.1186/s12865-025-00749-w.
由[病原体名称未给出]引起的泌尿生殖系统血吸虫病在全球影响超过1亿人，而在流行地区，其潜在的长期遗传和免疫后果尚不清楚。本研究调查了尼日利亚一个高度流行地区感染个体的遗传损伤和免疫失调情况。
与来自尼日利亚奥约州阿蒂斯博地方政府辖区的未感染对照相比，量化确诊感染[病原体名称未给出]个体的遗传损伤标志物并表征其免疫系统改变。
本横断面研究纳入了240名年龄在15至65岁之间的参与者（120名感染者，120名对照），采用多阶段整群抽样法进行选择。使用彗星试验、微核试验和染色体畸变分析评估遗传损伤。免疫分析包括Th1/Th2细胞因子、免疫球蛋白和补体成分。多变量回归模型确定了遗传损伤的独立预测因素。
感染者的遗传损伤明显升高：彗星尾矩为15.7±4.2，而对照为6.3±2.1（科恩d值=2.80，P<0.001）；微核频率为每1000个细胞中8.4±2.7个，而对照为3.1±1.2个（d值=2.41，P<0.001）；染色体异常率为12.3%，而对照为4.1%（P<0.001）。明显的Th2极化很明显，IL-4增加了4.1倍，IL-5增加了4.6倍，IL-13增加了4.1倍，而IFN-γ降低了65%（所有P<0.001，经FDR校正）。在调整年龄、体重指数、血红蛋白和性别后，[病原体名称未给出]感染独立预测遗传损伤（β=8.42，95%置信区间：7.51–9.33，P<0.001），解释了尾矩值方差的73%。
[病原体名称未给出]感染会导致大量遗传损伤和以Th2为主的免疫失调，可能产生严重的长期健康后果。这些发现为在流行人群中加强控制措施、加强治疗后监测和癌症监测计划提供了科学依据。
在线版本包含可在10.1186/s12865-025-00749-w获取的补充材料。
