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

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 infectio...

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Published in:PLoS neglected tropical diseases Vol. 16; no. 10; p. e0010878
Main Authors: Cortés, Alba, Martin, John, Rosa, Bruce A, Stark, Klara A, Clare, Simon, McCarthy, Catherine, Harcourt, Katherine, Brandt, Cordelia, Tolley, Charlotte, Lawley, Trevor D, Mitreva, Makedonka, Berriman, Matthew, Rinaldi, Gabriel, Cantacessi, Cinzia
Format: Journal Article
Language:English
Published: United States Public Library of Science 24-10-2022
Public Library of Science (PLoS)
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Summary: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.
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The authors declare that they have no competing interests
Current address: Department of Life Sciences, Aberystwyth University, Aberystwyth, United Kingdom
Current address: Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom
ISSN:1935-2735
1935-2727
1935-2735
DOI:10.1371/journal.pntd.0010878