{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T10:02:14Z","timestamp":1790676134861,"version":"4.1.0"},"reference-count":151,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T00:00:00Z","timestamp":1790640000000},"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. Cell. Infect. Microbiol."],"abstract":"<jats:p>\n                    STAT3 is a central mediator of pro-survival signaling within the STAT family, functioning through both canonical transcriptional activity and noncanonical mechanisms. As a pleiotropic regulator, STAT3 integrates cytokine, growth factor, and stress signals to coordinate diverse cellular processes, including epithelial architecture, T cell development, macrophage polarization, apoptosis, metabolism, and inflammation-associated wound healing. This integrative capacity positions STAT3 as a critical signaling hub at the interface of tissue homeostasis and immune regulation. Dysregulated STAT3 activity is strongly associated with cancer and chronic inflammatory disease. Notably, an increasing number of bacterial pathogens exploit STAT3 to facilitate infection and persistence. By targeting this central hub, pathogens reprogram host survival, metabolic, and immune pathways to create a permissive intracellular environment. In this review, we examine the molecular architecture of STAT3 signaling, its role in coordinating cellular programs, and the diverse mechanisms by which bacterial pathogens, including\n                    <jats:italic>Ehrlichia chaffeensis<\/jats:italic>\n                    ,\n                    <jats:italic>Helicobacter pylori<\/jats:italic>\n                    ,\n                    <jats:italic>Chlamydia<\/jats:italic>\n                    spp., and\n                    <jats:italic>Salmonella<\/jats:italic>\n                    spp., exploit STAT3 to promote infection.\n                  <\/jats:p>","DOI":"10.3389\/fcimb.2026.1826683","type":"journal-article","created":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T09:45:26Z","timestamp":1790675126000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Cellular signaling meets bacterial infection: the integrative role of STAT3"],"prefix":"10.3389","volume":"16","author":[{"given":"Jaclyn R.","family":"McCoy","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Texas Medical Branch","place":["Galveston, TX, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kayleigh H.","family":"Weinstein","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Texas Medical Branch","place":["Galveston, TX, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paityn A.","family":"Warwick","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Texas Medical Branch","place":["Galveston, TX, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jere W.","family":"McBride","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Texas Medical Branch","place":["Galveston, TX, United States"]},{"name":"Department of Microbiology and Immunology, University of Texas Medical Branch","place":["Galveston, TX, United States"]},{"name":"Center for Biodefense and Emerging Infectious Diseases, University of Texas Medical Branch","place":["Galveston, TX, United States"]},{"name":"Sealy Institute for Vaccine Sciences, University of Texas Medical Branch","place":["Galveston, TX, United States"]},{"name":"Institute for Human Infections and Immunity, University of Texas Medical Branch","place":["Galveston, TX, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,29]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"254","DOI":"10.1038\/cr.2008.18","article-title":"STAT3 as a target for inducing apoptosis in solid and hematological tumors","volume":"18","author":"Al Zaid Siddiquee","year":"2008","journal-title":"Cell Res."},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2024.1400348","article-title":"JAK inhibitors to treat STAT3 gain-of-function: a single-center report and literature review","volume":"15","author":"Atschekzei","year":"2024","journal-title":"Front. 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