{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T14:35:44Z","timestamp":1787841344694,"version":"build-2784847793"},"posted":{"date-parts":[[2026,8,25]]},"group-title":"Immunology","reference-count":67,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,8,25]],"date-time":"2026-08-25T00:00:00Z","timestamp":1787616000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.biorxiv.org\/about\/FAQ#license"}],"funder":[{"award":["R24DK110499"],"award-info":[{"award-number":["R24DK110499"]}],"id":[{"id":"https:\/\/ror.org\/001d55x84","id-type":"ROR","asserted-by":"publisher"}]},{"DOI":"10.13039\/100009576","name":"Kenneth Rainin Foundation","doi-asserted-by":"crossref","award":["Innovator Awards"],"award-info":[{"award-number":["Innovator Awards"]}],"id":[{"id":"10.13039\/100009576","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,8,25]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  The gut microbiota profoundly shapes intestinal immunity through the production of small-molecule metabolites; yet in inflammatory bowel diseases (IBD), where the microbial metabolome is substantially altered, the identities and immunological functions of most disease-associated metabolites remain unknown. Here, we integrate untargeted fecal metabolomics from two independent IBD patient cohorts with gnotobiotic mouse metabolomic data to identify N-acyl putrescines as a class of microbiome-associated metabolites consistently enriched in both Crohn\u2019s disease (CD) and ulcerative colitis (UC). Among these, N-oleoylputrescine (NOP) induces potent and selective transcriptional responses in bone marrow-derived dendritic cells (BMDCs) and colonic organoids, establishing it as the primary immunomodulatory candidate in this metabolite class.\n                  <jats:italic>Enterocloster<\/jats:italic>\n                  species harboring nonribosomal peptide synthetase (NRPS) biosynthetic gene clusters produce NOP via conjugation of oleic acid with putrescine, confirmed by isotope-tracing in vitro and germ-free mouse mono-colonization in vivo. NOP suppresses five core IBD-associated inflammatory pathways in mouse dendritic cells and human monocytes, reduces gene signatures of histologic inflammation and IBD therapy non-response, and ameliorates colitis in four murine models. NOP dampens NF-\u03baB activation and iNOS expression in myeloid cells and suppresses type 1 immune responses through a T cell-intrinsic mechanism. The enrichment of NOP in IBD despite its anti-inflammatory activity supports a holobiont defense hypothesis: that the gut microbiota mounts a compensatory metabolic response to intestinal inflammation that may contribute to the restoration of organismal homeostasis.\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>In Brief<\/jats:title>\n                  <jats:p>\n                    Bae et al. identify N-acyl putrescines as gut microbiota-associated metabolites enriched in IBD and demonstrate that N-oleoylputrescine (NOP), produced by\n                    <jats:italic>Enterocloster<\/jats:italic>\n                    species via NRPS biosynthetic machinery, broadly suppresses innate and adaptive inflammatory programs and ameliorates colitis in mice, supporting a holobiont defense hypothesis for microbiota-mediated immunomodulation.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Highlights<\/jats:title>\n                  <jats:list list-type=\"bullet\">\n                    <jats:list-item>\n                      <jats:p>N-acyl putrescines are microbiome-associated metabolites enriched in IBD feces across two independent human cohorts<\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>\n                        <jats:italic>Enterocloster<\/jats:italic>\n                        species harboring NRPS biosynthetic gene clusters produce NOP via oleic acid\u2013 putrescine conjugation\n                      <\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>NOP suppresses NF-\u03baB, iNOS, and IBD therapy non-response gene signatures in mouse and human myeloid cells<\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>NOP ameliorates colitis in four distinct murine models and suppresses type 1 immunity via a T cell-intrinsic mechanism<\/jats:p>\n                    <\/jats:list-item>\n                  <\/jats:list>\n                <\/jats:sec>","DOI":"10.64898\/2026.08.24.746719","type":"posted-content","created":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T03:55:21Z","timestamp":1787716521000},"source":"Crossref","is-referenced-by-count":0,"title":["Microbial-associated acylated putrescines as immunomodulatory molecules in inflammatory bowel diseases"],"prefix":"10.64898","author":[{"given":"Sena","family":"Bae","sequence":"first","affiliation":[{"name":"Department of Immunology & Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA"},{"name":"Harvard T.H. Chan Microbiome in Public Health Center, Boston, MA 02115, USA"},{"name":"Infectious Disease and Microbiome Program, Broad Institute of MIT and Harvard, Cambridge, MA 02114, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julian","family":"Avila-Pacheco","sequence":"additional","affiliation":[{"name":"Metabolomics Platform, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Slater L.","family":"Clay","sequence":"additional","affiliation":[{"name":"Department of Immunology & Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA"},{"name":"Harvard T.H. Chan Microbiome in Public Health Center, Boston, MA 02115, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sunghee","family":"Bang","sequence":"additional","affiliation":[{"name":"Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School and Blavatnik Institute, Boston, MA 02115, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Milcah C.","family":"Scott","sequence":"additional","affiliation":[{"name":"Department of Immunology & Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA"},{"name":"Harvard T.H. Chan Microbiome in Public Health Center, Boston, MA 02115, USA"},{"name":"Infectious Disease and Microbiome Program, Broad Institute of MIT and Harvard, Cambridge, MA 02114, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natalia","family":"Andreeva","sequence":"additional","affiliation":[{"name":"Department of Immunology & Infectious Diseases, Harvard T.H. 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