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However, the influence of specific microbes on commensal gut microbiota osteoimmunoregulatory actions is unknown. We have shown previously that the commensal gut microbiota enhances T\n                    <jats:sub>H<\/jats:sub>\n                    17\/IL17A immune response effects in marrow and liver that have procatabolic\/antianabolic actions in the skeleton. Segmented filamentous bacteria (SFB), a specific commensal gut bacterium within phylum Firmicutes, potently induces T\n                    <jats:sub>H<\/jats:sub>\n                    17\/IL17A\u2010mediated immunity. The study purpose was to delineate the influence of SFB on commensal gut microbiota immunomodulatory actions regulating normal postpubertal skeletal development. Two murine models were utilized: SFB\u2010monoassociated mice versus germ\u2010free (GF) mice and specific\u2010pathogen\u2010free (SPF) mice +\/\u2212 SFB. SFB colonization was validated by 16S rDNA analysis, and SFB\u2010induced T\n                    <jats:sub>H<\/jats:sub>\n                    17\/IL17A immunity was confirmed by upregulation of\n                    <jats:italic>Il17a<\/jats:italic>\n                    in ileum and IL17A in serum. SFB\u2010colonized mice had an osteopenic trabecular bone phenotype, which was attributed to SFB actions suppressing osteoblastogenesis and enhancing osteoclastogenesis. Intriguingly, SFB\u2010colonized mice had increased expression of proinflammatory chemokines and acute\u2010phase reactants in the liver. Lipocalin\u20102 (LCN2), an acute\u2010phase reactant and antimicrobial peptide, was substantially elevated in the liver and serum of SFB\u2010colonized mice, which supports the notion that SFB regulation of commensal gut microbiota osteoimmunomodulatory actions are mediated in part through a gut\u2013liver\u2013bone axis. Proinflammatory T\n                    <jats:sub>H<\/jats:sub>\n                    17 and T\n                    <jats:sub>H<\/jats:sub>\n                    1 cells were increased in liver\u2010draining lymph nodes of SFB\u2010colonized mice, which further substantiates that SFB osteoimmune\u2010response effects may be mediated through the liver. SFB\u2010induction of\n                    <jats:italic>Il17a<\/jats:italic>\n                    in the gut and\n                    <jats:italic>Lcn2<\/jats:italic>\n                    in the liver resulted in increased circulating levels of IL17A and LCN2. Recognizing that IL17A and LCN2 support osteoclastogenesis\/suppress osteoblastogenesis, SFB actions impairing postpubertal skeletal development appear to be mediated through immunomodulatory effects in both the gut and liver. This research reveals that specific microbes critically impact commensal gut microbiota immunomodulatory actions regulating normal postpubertal skeletal growth and maturation. \u00a9 2020 The Authors.\n                    <jats:italic>JBMR Plus<\/jats:italic>\n                    published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.\n                  <\/jats:p>","DOI":"10.1002\/jbm4.10338","type":"journal-article","created":{"date-parts":[[2020,1,10]],"date-time":"2020-01-10T18:03:03Z","timestamp":1578679383000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["Specific Commensal Bacterium Critically Regulates Gut Microbiota Osteoimmunomodulatory Actions During Normal Postpubertal Skeletal Growth and Maturation"],"prefix":"10.1093","volume":"4","author":[{"given":"Jessica D","family":"Hathaway\u2010Schrader","sequence":"first","affiliation":[{"name":"Department of Oral Health Sciences College of Dental Medicine, Medical University of South Carolina  Charleston SC USA"},{"name":"Department of Pediatrics\u2010Division of Endocrinology College of Medicine, Medical University of South Carolina  Charleston SC USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicole A","family":"Poulides","sequence":"additional","affiliation":[{"name":"Department of Oral Health Sciences College of Dental Medicine, Medical University of South Carolina  Charleston SC USA"},{"name":"Department of Pediatrics\u2010Division of Endocrinology College of Medicine, Medical University of South Carolina  Charleston SC USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew D","family":"Carson","sequence":"additional","affiliation":[{"name":"Department of Oral Health Sciences College of Dental Medicine, Medical University of South Carolina  Charleston SC USA"},{"name":"Department of Pediatrics\u2010Division of Endocrinology College of Medicine, Medical University of South Carolina  Charleston SC USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joy E","family":"Kirkpatrick","sequence":"additional","affiliation":[{"name":"Department of Oral Health Sciences College of Dental Medicine, Medical University of South Carolina  Charleston SC USA"},{"name":"Department of Drug Discovery &amp; Biomedical Sciences College of Pharmacy, Medical University of South Carolina  Charleston SC USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amy J","family":"Warner","sequence":"additional","affiliation":[{"name":"Department of Oral Health Sciences College of Dental Medicine, Medical University of South Carolina  Charleston SC USA"},{"name":"Department of Pediatrics\u2010Division of Endocrinology College of Medicine, Medical University of South Carolina  Charleston SC USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brooks 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