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Temporal modulation of gene expression in a controlled Schistosoma mansoni human infection model

ABSTRACT: Background Schistosomiasis is caused by parasitic blood flukes of the genus Schistosoma. Despite ongoing mass drug administration efforts, the disease remains a major public health burden in endemic regions. A better understanding of early host responses to schistosomiasis is critical for developing effective vaccines and therapeutics. Methods We conducted a longitudinal transcriptomic study of peripheral blood samples from 30 Schistosoma-naïve volunteers participating in two controlled human infection trials with male-or female-only S. mansoni cercariae. Blood was collected at six time points over 20 weeks post-infection. Whole-transcriptome RNA sequencing and integrative analyses, including differential gene expression, gene set enrichment, protein interaction networks, co-expression clustering, and immune module profiling, were employed to characterize temporal modulation of genes related to immune responses. Results Robust and highly time-dependent transcriptional responses were observed, peaking at Week 4 post-infection. Differential gene expression and pathway analyses revealed activation of immune responses, including type I and II interferon signaling, chemokine-mediated pathways, and antigen presentation. Notably, both Th1 and Th2 signatures were evident at Week 4. Key immune hubs included IFNG, TNF, and IL1B, along with transcriptional regulators such as STAT1 and IRF7. Blood transcription module analysis further highlighted transient activation of interferon and plasma cell-related responses. Conclusions This study provides a comprehensive transcriptional map of early host responses to S. mansoni infection in humans. The findings underscore the central role of interferon pathways, early mixed Th1/Th2 polarization, and inflammation-associated gene signatures in shaping host response to S. mansoni infection. These insights may inform the rational design of vaccines and biomarkers for schistosomiasis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE313156 | GEO | 2025/12/16

REPOSITORIES: GEO

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Project description:Schistosomiasis, caused by infection with Schistosoma trematode parasites, is one of the deadliest neglected tropical diseases in the world. The Schistosoma lifecycle involves the miracidia infection of an intermediate molluscan host, such as Biomphalaria glabrata. Dispersing B. glabrata attractant chemicals has been considered a method of minimising host infections. The attractiveness of B. glabrata is known to be reduced following infection; however, it remained unclear how the duration of infection affects attractiveness. Identifying excretory-secretory proteins (ESPs) abundant in attractive snail conditioned water (SCW) may facilitate the identification of attractants. This study obtained SCW ESPs from naïve snails and at different time-points post-miracidia exposure (PME; 16h-, 1 week, 2 weeks and 3 weeks), to identify those ESPs mediating Schistosome mansoni miracidia behavioural changes. The ESPs were quantitatively identified from all SCW samples using a label-free proteomic method and genome-derived protein databases of B. glabrata and S. mansoni. We found that changes in miracidia behaviour were similar upon exposure to naïve and 3W-PME SCW, including increased circling and quantity of miracidia in the field of view. Of the ESPs identified, 21 were shared in SCW of naïve and 3W-PME, and considered attractant candidates, including acetylcholine-binding protein and immune-related proteins such as biomphalysins and thioester-containing protein 1. Some biological processes were exclusive to attractant candidates, including obsolete pathogenesis and transmembrane transport activity. This suggests that compromised production of these proteins may diminish host attractiveness to miracidia. Additionally, several immune proteins were identified exclusively at 16-PME and 1W-PME, providing further information into changing B. glabrata immune responses throughout infection. These findings provide a list of attractant candidates to potentially decrease B. glabrata infection and minimise schistosomiasis.

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Temporal modulation of gene expression in a controlled Schistosoma mansoni human infection model

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