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Although TTP deficiency is associated with systemic inflammation and microbial dysbiosis, the contribution of the gut microbiota to bone pathology remains poorly defined.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and methods<\/jats:title>\n                    <jats:p>We investigated whether the microbiome causally modulates osteoimmune mechanisms and bone microarchitecture in TTP-deficient mice. To isolate the effects of the microbiome, we utilized specific pathogen-free (SPF) and germ-free (GF) co-housing mouse models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Microbial transfer bidirectionally regulated systemic inflammation and the expansion of monocytic myeloid-derived suppressor cells (M-MDSCs), a population with potent osteoclastogenic capacity. Importantly, microbiota transfer was sufficient to induce osteoclast activation and a selective deterioration of trabecular bone microarchitecture in otherwise healthy mice, without affecting overall bone mass. Crucially, the transmission of these osteoimmune and skeletal phenotypes was microbiota-dependent; while a baseline genetic bone deficit persisted in GF TTP-deficient mice, the co-housing-induced M-MDSC expansion and trabecular bone alterations were not observed under GF conditions.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our findings identify a microbiota-dependent osteoimmune axis that amplifies inflammatory bone loss in TTP deficiency. This work establishes the gut microbiome as a mechanistic modifier of bone quality in genetically driven inflammatory disease and highlights microbial targeting as a potential therapeutic strategy for inflammatory bone loss.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s00774-026-01753-9","type":"journal-article","created":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T07:56:46Z","timestamp":1786953406000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Gut microbiota transmits osteoimmune dysregulation and exacerbates trabecular bone loss in tristetraprolin-deficient mice"],"prefix":"10.1007","author":[{"given":"Kyu Hwan","family":"Kwack","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiho","family":"Sohn","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lixia","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lu","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Reegan","family":"Mullaney","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yukitomo","family":"Arao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Perry J.","family":"Blackshear","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4519-8973","authenticated-orcid":false,"given":"Keith L.","family":"Kirkwood","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,8,17]]},"reference":[{"key":"1753_CR1","doi-asserted-by":"publisher","first-page":"1822","DOI":"10.1038\/s41591-019-0675-0","volume":"25","author":"D Furman","year":"2019","unstructured":"Furman D, Campisi J, Verdin E, Carrera-Bastos P, Targ S et al (2019) Chronic inflammation in the etiology of disease across the life span. 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