{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T09:00:51Z","timestamp":1790240451893,"version":"4.1.0"},"reference-count":49,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T00:00:00Z","timestamp":1789516800000},"content-version":"vor","delay-in-days":15,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T00:00:00Z","timestamp":1788220800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000072","name":"National Institute of Dental and Craniofacial Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000072","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Barrier Immunity"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Neonatal dysbiosis of the gut microbiota represents a critical environmental factor promoting obesity, but the underlying immunological mechanisms remain unknown. We show here that neonatal treatment of mice with broad\u2010spectrum antibiotics for the first 3\u00a0weeks of life (NeoATB) resulted in the development of obesity and metabolic abnormalities in adulthood. The NeoATB mice exhibited a permanent dysbiosis of gut microbiota, decreased CD4\n                    <jats:sup>+<\/jats:sup>\n                    Foxp3\n                    <jats:sup>+<\/jats:sup>\n                    regulatory T cells (Tregs), and increased proinflammatory Th1 cells in visceral adipose tissue (VAT). Mechanistically, neonatal antibiotic treatment resulted in increased intestinal permeability that allowed bacterial translocation into the VAT and liver and an increase in systemic LPS levels. Consequently, VAT CD11c\n                    <jats:sup>+<\/jats:sup>\n                    MHCII\n                    <jats:sup>+<\/jats:sup>\n                    cells were activated via the TLR4 pathway to increase IL\u201012\u2010triggered Th1\u2010inflammation. Moreover, the decrease in VAT Tregs in NeoATB mice was attributed to reduced infiltration of Tregs from the periphery, decreased expansion of adipose IL\u201033\u2010mediated ST2\n                    <jats:sup>+<\/jats:sup>\n                    Tregs, and reduced conversion of local Tregs from VAT CD4\n                    <jats:sup>+<\/jats:sup>\n                    CD25\n                    <jats:sup>\u2212<\/jats:sup>\n                    Foxp3\n                    <jats:sup>\u2212<\/jats:sup>\n                    T cells. Thus, we have revealed a previously unrecognized immunological link between neonatal microbiota dysbiosis and the development of obesity.\n                  <\/jats:p>","DOI":"10.1002\/dni2.70003","type":"journal-article","created":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T05:43:03Z","timestamp":1789623783000},"page":"147-164","source":"Crossref","is-referenced-by-count":0,"title":["Neonatal Exposure to Antibiotics Triggers Obesity in Adulthood by Permanent Microbiota Dysbiosis and Reduction of Adipose Regulatory T Cells"],"prefix":"10.1002","volume":"2","author":[{"given":"Peter","family":"Zanvit","sequence":"first","affiliation":[{"name":"Mucosal Immunology Section National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of Health  Bethesda Maryland USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junji","family":"Xu","sequence":"additional","affiliation":[{"name":"Mucosal Immunology Section National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of Health  Bethesda Maryland USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenjing","family":"Yang","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology Department of Medicine Northwestern University  Chicago Illinois USA"},{"name":"Department of Microbiology and Immunology University of Texas Medical Branch  Galveston Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nancy","family":"Guo","sequence":"additional","affiliation":[{"name":"Mucosal Immunology Section National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of Health  Bethesda Maryland USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tianming","family":"Yu","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology Department of Medicine Northwestern University  Chicago Illinois USA"},{"name":"Department of Microbiology and Immunology University of Texas Medical Branch  Galveston Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xue","family":"Jiao","sequence":"additional","affiliation":[{"name":"Mucosal Immunology Section National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of Health  Bethesda Maryland USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michaela","family":"Prochazkova","sequence":"additional","affiliation":[{"name":"Department of Transfusion Medicine, Center for Cellular Engineering NIH  Bethesda Maryland USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenwen","family":"Jin","sequence":"additional","affiliation":[{"name":"Mucosal Immunology Section National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of Health  Bethesda Maryland 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