The common mouse protozoa Tritrichomonas muris alters mucosal T cell homeostasis and colitis susceptibility

Author:

Escalante Nichole K.1ORCID,Lemire Paul2,Cruz Tleugabulova Mayra1,Prescott David12,Mortha Arthur3,Streutker Catherine J.2,Girardin Stephen E.2,Philpott Dana J.1ORCID,Mallevaey Thierry1ORCID

Affiliation:

1. Department of Immunology, University of Toronto, Toronto, Ontario M5S 1A8, Canada

2. Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario M5S 1A8, Canada

3. Department of Oncological Science, Icahn School of Medicine at Mount Sinai, New York, NY 10029

Abstract

The mammalian gastrointestinal tract hosts a diverse community of microbes including bacteria, fungi, protozoa, helminths, and viruses. Through coevolution, mammals and these microbes have developed a symbiosis that is sustained through the host’s continuous sensing of microbial factors and the generation of a tolerant or pro-inflammatory response. While analyzing T cell–driven colitis in nonlittermate mouse strains, we serendipitously identified that a nongenetic transmissible factor dramatically increased disease susceptibility. We identified the protozoan Tritrichomonas muris as the disease-exacerbating element. Furthermore, experimental colonization with T. muris induced an elevated Th1 response in the cecum of naive wild-type mice and accelerated colitis in Rag1−/− mice after T cell transfer. Overall, we describe a novel cross-kingdom interaction within the murine gut that alters immune cell homeostasis and disease susceptibility. This example of unpredicted microbial priming of the immune response highlights the importance of studying trans-kingdom interactions and serves as a stark reminder of the importance of using littermate controls in all mouse research.

Funder

Canadian Institutes of Health Research

Crohn’s and Colitis Foundation of Canada

Publisher

Rockefeller University Press

Subject

Immunology,Immunology and Allergy

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