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Protists protecting food tolerance.
Macy R Komnick1, Daria Esterházy1
1Committee on Immunology, University of Chicago, Chicago, IL, USA; Department of Pathology, University of Chicago, Chicago, IL, USA.
Trends in Immunology
|August 17, 2023
Summary
A newly discovered protist, Tritrichomonas arnold, protects mice from gluten intolerance caused by viral infections. This commensal organism counters virus-induced stress and immune cell activation, offering a novel protective mechanism against celiac disease triggers.
Area of Science:
- Immunology
- Microbiology
- Gastroenterology
Background:
- Celiac disease (CeD) is an immune disorder involving gluten intolerance.
- Enteric viral infections can trigger CeD in susceptible individuals, particularly in mice models.
- The mechanisms underlying virus-induced gluten intolerance are not fully understood.
Purpose of the Study:
- To investigate the protective role of commensal microorganisms against virus-induced gluten intolerance.
- To identify specific mechanisms by which commensals modulate host immune responses to viral infections and dietary antigens.
Main Methods:
- Utilized a mouse model of reovirus-induced gluten intolerance.
- Introduced the murine commensal protist Tritrichomonas arnold.
- Assessed epithelial stress markers and dendritic cell (DC) activation.
Main Results:
- Tritrichomonas arnold administration prevented reovirus-induced intolerance to dietary protein in mice.
- The protist counteracted virus-induced epithelial stress.
- T. arnold inhibited proinflammatory dendritic cell (DC) activation.
Conclusions:
- Murine commensal protists, like Tritrichomonas arnold, can confer protection against enteric virus-induced gluten intolerance.
- T. arnold mitigates CeD-like symptoms by modulating epithelial and immune responses.
- These findings highlight the potential of commensal microbes in managing immune-mediated gastrointestinal disorders.
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