{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,14]],"date-time":"2026-04-14T01:05:27Z","timestamp":1776128727968,"version":"3.50.1"},"reference-count":56,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,1,15]],"date-time":"2026-01-15T00:00:00Z","timestamp":1768435200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Periodontitis is clinically associated with inflammatory bowel disease (IBD), yet the shared cellular and molecular programs underpinning this oral\u2013gut inflammatory link remain incompletely defined.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We integrated bulk gingival transcriptomes from two periodontitis cohorts (GSE16134 and GSE10334) with single-cell RNA-seq data from IBD patients (51,322 cells, 18 samples). After standard quality control and batch-aware integration, we performed pseudobulk differential expression gene (DEG) analysis at the patient level to identify IBD-associated genes and intersected these with periodontitis-consensus DEGs to derive shared signatures. Cell-cell communication networks were inferred using CellChat, and gene set enrichment analysis were conducted to delineated inflammatory signaling. Myeloid subpopulations further resolved to characterize disease-associated functional states. Key findings were assessed in a dual-inflammation rodent model by immunohistochemistry.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We identified 188 common DEGs across the two periodontitis cohorts and 66 genes shared in IBD, which were predominantly enriched in immune compartments and motivated a focused analysis of myeloid cells. Communication analysis revealed extensive network remodeling in IBD, with myeloid populations acting as major signaling hubs. Myeloid subclustering highlighted inflammatory and chemokine-related states characterized by high\n                      <jats:italic>IL1B<\/jats:italic>\n                      expression. Among chemokines,\n                      <jats:italic>CXCL2<\/jats:italic>\n                      was prioritized because it showed consistent upregulation across bulk periodontitis transcriptomes and IBD myeloid states, and it aligned with prominent IL-1\u03b2\u2013chemokine signaling routes inferred from intercellular communication.\n                      <jats:italic>In vivo<\/jats:italic>\n                      , IL-1\u03b2 and CXCL2 signals were increased in the dual-inflammation model, supporting cross-disease consistency of this axis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our integrative analyses identify a shared, myeloid-centered IL-1\u03b2\/chemokine inflammatory program across periodontitis and IBD, which may contribute to the oral\u2013gut inflammatory axis. The IL1\u03b2\u2013CXCL2 pathway represents a potentially targetable signaling module, although functional blockade studies are required to establish therapeutic causality.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2025.1728773","type":"journal-article","created":{"date-parts":[[2026,1,15]],"date-time":"2026-01-15T06:24:22Z","timestamp":1768458262000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Unveiling the IL-1\u03b2\/CXCL2 axis: a shared therapeutic target in periodontitis and inflammatory bowel disease"],"prefix":"10.3389","volume":"16","author":[{"given":"Zhongyi","family":"Gu","sequence":"first","affiliation":[{"name":"Department of Periodontology, The Affiliated Yantai Stomatological Hospital, Binzhou Medical University","place":["Yantai, 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Stomatological Hospital, Binzhou Medical University","place":["Yantai, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yucun","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, The Affiliated Yantaishan Hospital, Binzhou Medical University","place":["Yantai, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Caiqing","family":"Qiu","sequence":"additional","affiliation":[{"name":"Department of Periodontology, The Affiliated Yantai Stomatological Hospital, Binzhou Medical University","place":["Yantai, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1965","published-online":{"date-parts":[[2026,1,15]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1126\/sciadv.adg3390","article-title":"Microbial \u03b2-glucuronidases drive human periodontal disease etiology","volume":"9","author":"Lietzan","year":"2023","journal-title":"Sci 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