The gut microbial metabolic capacity of microbiome-humanized vs. wild type rodents reveals a likely dual role of intestinal bacteria in hepato-intestinal schistosomiasis

Alba Cortés, University of Cambridge
John Martin, Universitat de València
Bruce A. Rosa, Universitat de València
Klara A. Stark, University of Cambridge
Simon Clare, University of Cambridge
Catherine McCarthy, Wellcome Genome Campus
Katherine Harcourt, Wellcome Genome Campus
Cordelia Brandt, Wellcome Genome Campus
Charlotte Tolley, Wellcome Genome Campus
Trevor D. Lawley, Wellcome Genome Campus
Makedonka Mitreva, Washington University School of Medicine in St. Louis
Matthew Berriman, Wellcome Genome Campus
Gabriel Rinaldi, Wellcome Genome Campus
Cinzia Cantacessi, University of Cambridge


Increasing evidence shows that the host gut microbiota might be involved in the immunological cascade that culminates with the formation of tissue granulomas underlying the pathophysiology of hepato-intestinal schistosomiasis. In this study, we investigated the impact of Schistosoma mansoni infection on the gut microbial composition and functional potential of both wild type and microbiome-humanized mice. In spite of substantial differences in microbiome composition at baseline, selected pathways were consistently affected by parasite infection. The gut microbiomes of infected mice of both lines displayed, amongst other features, enhanced capacity for tryptophan and butyrate production, which might be linked to the activation of mechanisms aimed to prevent excessive injuries caused by migrating parasite eggs. Complementing data from previous studies, our findings suggest that the host gut microbiome might play a dual role in the pathophysiology of schistosomiasis, where intestinal bacteria may contribute to egg-associated pathology while, in turn, protect the host from uncontrolled tissue damage.