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The mechanisms underlying this immune subversion remain incompletely understood, but likely involve specific bacterial effector proteins. Here, we identify CT181 as a novel effector that binds to Mcl-1, a key regulator of neutrophil survival. While a\n                      <jats:italic toggle=\"yes\">C.t<\/jats:italic>\n                      . CT181 mutant exhibited only modest defects in epithelial cell replication and inclusion development, it was required for\n                      <jats:italic toggle=\"yes\">C.t<\/jats:italic>\n                      . survival in neutrophils, which correlated with elevated Mcl-1 levels in cells infected with wild-type\n                      <jats:italic toggle=\"yes\">C.t<\/jats:italic>\n                      . Using a murine infection model, we demonstrate that CT181 contributes to\n                      <jats:italic toggle=\"yes\">C.t<\/jats:italic>\n                      . colonization and inflammatory cytokine production\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      . Our findings establish CT181 as the first bacterial effector protein known to bind Mcl-1 and show that it is associated with prolonged neutrophil survival, revealing a novel strategy by which\n                      <jats:italic toggle=\"yes\">C.t<\/jats:italic>\n                      . promotes immune dysregulation, facilitating bacterial persistence while driving\n                      <jats:italic toggle=\"yes\">C.t<\/jats:italic>\n                      . pathogenesis.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        <jats:italic toggle=\"yes\">Chlamydia trachomatis<\/jats:italic>\n                        is an obligate intracellular pathogen that must evade early immune defenses to establish infection. This study identifies CT181 as a previously undescribed secreted effector that associates with the host pro-survival protein Mcl-1 and is linked to prolonged neutrophil survival during infection. Neutrophils, which normally undergo rapid apoptosis, persist longer when infected with wild-type\n                        <jats:italic toggle=\"yes\">C. trachomatis<\/jats:italic>\n                        , whereas loss of CT181 reduces bacterial survival in these cells. In a mouse model of infection, the CT181 mutant exhibits reduced bacterial burden and diminished inflammatory responses, including neutrophil recruitment and cytokine production. Together, these findings highlight CT181 as a bacterial factor that contributes to host cell survival and immune modulation during\n                        <jats:italic toggle=\"yes\">C. trachomatis<\/jats:italic>\n                        infection, underscoring the complex strategies used by intracellular pathogens to persist within the host.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.00357-26","type":"journal-article","created":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T13:00:46Z","timestamp":1778850046000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":1,"title":["The\n                    <i>Chlamydia trachomatis<\/i>\n                    -secreted effector protein CT181 binds to Mcl-1 and prolongs neutrophil survival"],"prefix":"10.1128","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0855-7041","authenticated-orcid":true,"given":"Robert","family":"Faris","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/036jqmy94","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, University of Iowa Carver College of Medicine","place":["Iowa City, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rebecca","family":"Koch","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00fbnyb24","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology, Biocenter, University of W\u00fcrzburg","place":["W\u00fcrzburg, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paige","family":"McCaslin","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/036jqmy94","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, University of Iowa Carver College of Medicine","place":["Iowa City, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naveen","family":"Challagundla","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00fbnyb24","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology, Biocenter, University of W\u00fcrzburg","place":["W\u00fcrzburg, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7992-004X","authenticated-orcid":true,"given":"Brianna","family":"Steiert","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/036jqmy94","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, University of Iowa Carver College of Medicine","place":["Iowa City, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shelby E.","family":"Andersen","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/036jqmy94","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, University of Iowa Carver College of Medicine","place":["Iowa City, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alix","family":"McCullough","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/036jqmy94","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, University of Iowa Carver College of Medicine","place":["Iowa City, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Parker","family":"Smith","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/036jqmy94","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, University of Iowa Carver College of Medicine","place":["Iowa City, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. 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