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Although <jats:italic>Chlamydia (C.) trachomatis<\/jats:italic> is associated with adverse pregnancy outcomes the pathogenic effects on maternal decidua contributing to adverse events are not understood. This study examined how <jats:italic>C. trachomatis<\/jats:italic> antigen affects cell signaling, cell death, and inflammation in the decidua.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Primary decidua cells (pDECs) from term, not\u2010in\u2010labor, fetal membrane\u2010decidua were cultured using the following conditions: (1) control \u2013 standard cell culture conditions, (2) 100\u00a0ng\/ml or (3) 200\u00a0ng\/ml of <jats:italic>C. trachomatis<\/jats:italic> antigen to model decidual cell infection in vitro. Differential expression of Toll\u2010like receptor (TLR) 4 (receptor for <jats:italic>C. trachomatis<\/jats:italic> antigen), signaling pathway markers phosphorylated TGF\u2010Beta Activated Kinase 1 (PTAB1), TAB1, phosphorylated p38 mitogen\u2010activated protein kinases (Pp38 MAPK), and p38 MAPK (western blot), decidual cell apoptosis and necrosis (flow cytometry), and inflammation (ELISA for cytokines) were determined in cells exposed to <jats:italic>C. trachomatis<\/jats:italic> antigen. <jats:italic>T<\/jats:italic>\u2010test was used to assess statistical significance (<jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.05).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:italic>C. trachomatis<\/jats:italic> antigen significantly induced expression of TLR4 (<jats:italic>p<\/jats:italic>\u00a0=\u00a00.03) and activation of TAB1 (<jats:italic>p<\/jats:italic>\u00a0=\u00a00.02) compared to controls. However, it did not induce p38 MAPK activation. In addition, pDECs maintained their stromal cell morphology when exposed to <jats:italic>C. trachomatis<\/jats:italic> antigen showing no signs of apoptosis and\/or necrosis but did induce pro\u2010inflammatory cytokine interleukin (IL)\u20106 (100\u00a0ng\/ml: <jats:italic>p<\/jats:italic>\u00a0=\u00a00.02 and 200\u00a0ng\/ml: <jats:italic>p<\/jats:italic>\u00a0=\u00a00.03), in pDECs compared to controls.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Prenatal <jats:italic>C. trachomatis<\/jats:italic> infection can produce antigens that induce TLR4\u2010TAB1 signaling and IL\u20106 inflammation independent of Pp38 MAPK and apoptosis and necrosis. This suggests that <jats:italic>C. trachomatis<\/jats:italic> can imbalance decidual inflammatory homeostasis, potentially contributing to adverse events during pregnancy.<\/jats:p><\/jats:sec>","DOI":"10.1111\/aji.13664","type":"journal-article","created":{"date-parts":[[2022,12,10]],"date-time":"2022-12-10T07:25:45Z","timestamp":1670657145000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Chlamydia trachomatis antigen induces TLR4\u2010TAB1\u2010mediated inflammation, but not cell death, in maternal decidua cells"],"prefix":"10.1111","volume":"89","author":[{"given":"Briana","family":"Ortiz","sequence":"first","affiliation":[{"name":"School of Medicine The University of Texas Medical Branch at Galveston  Galveston Texas USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ashley","family":"Driscoll","sequence":"additional","affiliation":[{"name":"School of Medicine The University of Texas 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