GUT MICROBIOTA a Protective Protozoan in Mucosal Infection

RESEARCH HIGHLIGHTS

Nature Reviews Gastroenterology & Hepatology | Published online 19 Oct 2016; doi:10.1038/nrgastro.2016.174

GUT MICROBIOTA A protective protozoan in mucosal infection

A novel mutualistic host–protozoan presence of a unicellular flagellated interaction has been reported in a microorganism that resembled a new study published in Cell. The parabasalid protozoan parasite in findings highlight how a commensal the in-house mice, which closely protist Tritrichomonas musculis adhered to the intestinal epithelium. (termed T. mu) can modulate Ribosomal DNA sequencing gut mucosal immunity in confirmed that this microorganism mice, protecting the host from (now termed T. mu) had not enteric infection. been characterized previously, “The finding was total serendipity, being similar to but distinct from we observed that wild-type C57BL/6 Tritrichomonas muris. Screening mice that were bred in-house had of faecal samples from 188 healthy Image courtesy of A. Mortha and A. Chudnovskiy. increased numbers of immune cells individuals from Colombia with no and increased levels of inflammatory gastrointestinal infections and from colorectal cancer (increased cytokines compared to animals 98 Giardia-positive samples from tumour burden in Apcmin/+ mice) in obtained from a commercial vendor,” individuals from South America, experimental settings. By contrast, explains author Miriam Merad. Africa, Europe and Asia revealed the T. mu-modulated immune “This phenotype was exclusively the presence of the T. mu human response protected mice from confined to the large intestine,” homologue Dientamoeba fragilis. Salmonella infection. she notes, adding that despite Crucially, the investigators “These studies emphasize further increased basal levels of intestinal found that colonization with T. mu the importance of nonbacterial inflammation these in-house modulated gut mucosal immunity species to our studies of the mice did not display tissue injury. in mice, activating the host epithelial microbiome,” concludes Merad. These observations prompted the inflammasome and inducing IL-18 The researchers are now analysing researchers to find out the cause production. This epithelial-derived the contributions of the human

of this inflammation, suspecting IL-18 promoted T helper (TH)1 and T. mu homologues in human gut

that there might be a microbial TH17 immunity via dendritic cells. tissue immunity. component as both groups of mice Interestingly, immune modulation Katrina Ray had the same genetic background. via T. mu colonization had different

Merad and colleagues first outcomes in different settings. ORIGINAL ARTICLE Chudnovskiy, A. et al. assessed faecal material from T. mu colonization worsened Host-protozoan interactions protect from the different mouse populations. T-cell-mediated colitis (more mucosal infections through activation of the inflammasome. Cell 167, 1–13 (2016) Microscopic analysis revealed the severe disease scores) and sporadic