1. The common mouse protozoa Tritrichomonas muris alters mucosal T cell homeostasis and colitis susceptibility.
- Author
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Escalante NK, Lemire P, Cruz Tleugabulova M, Prescott D, Mortha A, Streutker CJ, Girardin SE, Philpott DJ, and Mallevaey T
- Subjects
- Animals, Colitis genetics, Colitis parasitology, Colitis pathology, Disease Susceptibility immunology, Disease Susceptibility parasitology, Disease Susceptibility pathology, Homeodomain Proteins genetics, Homeodomain Proteins immunology, Intestinal Mucosa parasitology, Intestinal Mucosa pathology, Mice, Mice, Knockout, Colitis immunology, Immunity, Mucosal, Intestinal Mucosa immunology, T-Lymphocytes immunology, Tritrichomonas immunology
- 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., (© 2016 Escalante et al.)- Published
- 2016
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