{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T15:19:06Z","timestamp":1785424746434,"version":"3.56.0"},"reference-count":55,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T00:00:00Z","timestamp":1781049600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T00:00:00Z","timestamp":1781049600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"name":"NIH","award":["K22-AI166029"],"award-info":[{"award-number":["K22-AI166029"]}]},{"name":"NIH","award":["R01-AI144016-01"],"award-info":[{"award-number":["R01-AI144016-01"]}]},{"name":"UW-Madison","award":["SciMed Graduate Research Scholars Fellowship"],"award-info":[{"award-number":["SciMed Graduate Research Scholars Fellowship"]}]},{"name":"Food Research Institute","award":["Carol L. Deibel Distinguished Graduate Fellowship in Probiotic Research from the Food Research Institute"],"award-info":[{"award-number":["Carol L. Deibel Distinguished Graduate Fellowship in Probiotic Research from the Food Research Institute"]}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mBio"],"published-print":{"date-parts":[[2026,6,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Intestinal protists are emerging as key modulators of host immunity and microbial ecology, yet their impact on mammalian hosts remains poorly defined. Here, we investigated the role of two distinct protists, the amoeba\n                      <jats:italic toggle=\"yes\">Entamoeba muris<\/jats:italic>\n                      , and the parabasalid,\n                      <jats:italic toggle=\"yes\">Tritrichomonas<\/jats:italic>\n                      , to determine how they shape gut immunity\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      individually and together. Unlike the well-characterized inducer of type 2 immunity,\n                      <jats:italic toggle=\"yes\">Tritrichomonas<\/jats:italic>\n                      , which activates the tuft cell\u2013IL-25\u2013ILC2 circuit in the small intestine,\n                      <jats:italic toggle=\"yes\">E. muris<\/jats:italic>\n                      failed to elicit robust immune responses in the intestine or colon. However, the introduction of\n                      <jats:italic toggle=\"yes\">E. muris<\/jats:italic>\n                      into mice naturally colonized by\n                      <jats:italic toggle=\"yes\">Tritrichomonas<\/jats:italic>\n                      spp., or co-infection with\n                      <jats:italic toggle=\"yes\">E. muris<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">Tritrichomonas<\/jats:italic>\n                      spp. reduced\n                      <jats:italic toggle=\"yes\">Tritrichomonas<\/jats:italic>\n                      -induced type-2 response in the small intestine and\n                      <jats:italic toggle=\"yes\">Tritrichomonas-<\/jats:italic>\n                      dependent immune activation in the colon. Our data suggest that\n                      <jats:italic toggle=\"yes\">E. muris<\/jats:italic>\n                      may limit the abundance of\n                      <jats:italic toggle=\"yes\">Tritrichomonas<\/jats:italic>\n                      spp., with reduced protist loads in the cecum specifically correlating with diminished tuft cell activation. We also identified sex-specific differences in the intestinal response to\n                      <jats:italic toggle=\"yes\">Tritrichomonas<\/jats:italic>\n                      spp., which have not previously been reported. Taken together, these findings reveal that the presence of\n                      <jats:italic toggle=\"yes\">E. muris<\/jats:italic>\n                      reduces\n                      <jats:italic toggle=\"yes\">Tritrichomonas<\/jats:italic>\n                      -dependent activation of type 2 immunity in the small intestine, even when both protists can be detected in the cecum, without triggering overt inflammation. This work provides a framework for understanding how protists interact within the gut ecosystem and shape mucosal immunity in the absence of pathogenicity.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>\n                      Single-cell parasites called protists are common in mammalian intestinal tracts, yet their modulation of the host immune response and interactions with each other remain poorly defined. Here, we investigated the role of two protists,\n                      <jats:italic toggle=\"yes\">Entamoeba<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">Tritrichomonas<\/jats:italic>\n                      , to determine how they shape gut immunity individually and together. Unlike the well-characterized inducer of type 2 immunity,\n                      <jats:italic toggle=\"yes\">Tritrichomonas<\/jats:italic>\n                      , which activates the tuft cell circuit,\n                      <jats:italic toggle=\"yes\">Entamoeba<\/jats:italic>\n                      failed to elicit a robust immune response. The introduction of\n                      <jats:italic toggle=\"yes\">Entamoeba<\/jats:italic>\n                      into mice naturally colonized by\n                      <jats:italic toggle=\"yes\">Tritrichomonas<\/jats:italic>\n                      , or co-infection with Entamoeba and Tritrichomonas, reduced the\n                      <jats:italic toggle=\"yes\">Tritrichomonas<\/jats:italic>\n                      -induced immune response. Our data suggest that\n                      <jats:italic toggle=\"yes\">Entamoeba<\/jats:italic>\n                      limits the abundance of\n                      <jats:italic toggle=\"yes\">Tritrichomonas<\/jats:italic>\n                      , correlating with diminished tuft cell activation. We also identified sex-specific differences in the intestinal response to\n                      <jats:italic toggle=\"yes\">Tritrichomonas<\/jats:italic>\n                      . These findings show that\n                      <jats:italic toggle=\"yes\">Entamoeba<\/jats:italic>\n                      reduces\n                      <jats:italic toggle=\"yes\">Tritrichomonas<\/jats:italic>\n                      -dependent activation of type 2 immunity without triggering much inflammation. It helps our understanding of how protists interact within the gut and shape immunity without disease.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.00802-26","type":"journal-article","created":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T13:01:59Z","timestamp":1779109319000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Competition between commensal protists shapes gut mucosal immunity in mice"],"prefix":"10.1128","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6247-1252","authenticated-orcid":false,"given":"Marienela Y.","family":"Heredia","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01y2jtd41","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Medical Microbiology and Immunology, University of Wisconsin\u2014Madison School of Medicine and Public Health","place":["Madison, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul A.","family":"Kuehnert","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01y2jtd41","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Pediatrics, University of Wisconsin\u2014Madison School of Medicine and Public Health","place":["Madison, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kylie","family":"March","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01y2jtd41","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Pediatrics, University of Wisconsin\u2014Madison School of Medicine and Public Health","place":["Madison, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9362-8088","authenticated-orcid":true,"given":"Laura 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