article · The Journal of Immunology
This study investigated why some individuals infected with *Schistosoma mansoni* develop advanced periportal fibrosis, a severe liver condition. Researchers evaluated 795 inhabitants of a Sudanese village where the infection is common, finding that 12% had advanced fibrosis, with 35% of these showing signs of portal hypertension. Age, gender, and infection levels were significantly linked to hepatic fibrosis. By measuring cytokine levels in 99 subjects, the study found that high levels of interferon-gamma (IFN-γ) were associated with a reduced risk of fibrosis, while high levels of tumour necrosis factor-alpha (TNF-α) were linked to an increased risk. These findings suggest that IFN-γ protects against fibrosis, and TNF-α may worsen the disease.
Understanding why some people develop severe liver fibrosis from *Schistosoma mansoni* infection is crucial. Identifying specific immune molecules like IFN-γ and TNF-α that either protect or worsen the disease could lead to new ways to predict, prevent, or treat this debilitating condition, improving health outcomes for affected populations.
This early-stage research identifies specific cytokine biomarkers, IFN-γ and TNF-α, that are associated with protection or aggravation of periportal fibrosis in *Schistosoma mansoni* infection. These findings could potentially inform the development of diagnostic tools to identify individuals at higher risk of severe disease or contribute to the discovery of new therapeutic targets for drug development aimed at modulating the immune response to prevent or treat fibrosis. The abstract does not indicate a specific product or a near-market application.
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Hepatic periportal fibrosis, which affects 5-10% of subjects infected by Schistosoma mansoni, is caused by the T cell-dependent granuloma that develop around schistosome eggs. Experimental models of infection have shown that granuloma and fibrosis are tightly regulated by cytokines. However, it is unknown why advanced periportal fibrosis occurs only in certain subjects. The goal of the present study was to evaluate the cytokine response of S. mansoni-infected subjects with advanced liver disease in an attempt to relate susceptibility to periportal fibrosis with an abnormal production of cytokines that regulate granuloma and fibrosis. Fibrosis was evaluated by ultrasound on 795 inhabitants of a Sudanese village in which S. mansoni is endemic: advanced periportal fibrosis was observed in 12% of the population; 35% of the affected subjects exhibited signs of portal hypertension. Age (odds ratio (OR), 11.5), gender (OR, 4.2), and infection levels (OR, 2.2) were significantly (p < or = 0.01) associated with hepatic fibrosis. Cytokines produced by egg-stimulated blood mononuclear cells from 99 subjects were measured (75 with no or mild fibrosis; 24 subjects with advanced fibrosis). Multivariate analysis of cytokine levels showed that high IFN-gamma levels were associated with a marked reduction of the risk of fibrosis (p = 0.01; OR, 0.1); in contrast, high TNF-alpha levels were associated with an increased risk (p = 0.05; OR, 4.6) of periportal fibrosis. Moreover, infection levels were negatively associated with IFN-gamma production. These results with observations in experimental models strongly suggest that IFN-gamma plays a key role in the protection of S. mansoni-infected patients against periportal fibrosis, whereas TNF-alpha may aggravate the disease.
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DOI: 10.4049/jimmunol.169.2.929
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