{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T01:15:45Z","timestamp":1788225345071,"version":"build-2803163510"},"reference-count":53,"publisher":"American Society for Microbiology","issue":"7","license":[{"start":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T00:00:00Z","timestamp":1783382400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T00:00:00Z","timestamp":1783382400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Microbiol Spectr"],"published-print":{"date-parts":[[2026,7,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Chlamydia trachomatis<\/jats:italic>\n                      (\n                      <jats:italic toggle=\"yes\">Ct<\/jats:italic>\n                      )\n                      <jats:italic toggle=\"yes\">,<\/jats:italic>\n                      an obligate intracellular pathogen, manipulates host cell death pathways to establish infection. Although ferroptosis\u2014an iron-dependent cell death process marked by lipid peroxidation\u2014constitutes an antimicrobial defense mechanism, its regulation during\n                      <jats:italic toggle=\"yes\">Ct<\/jats:italic>\n                      infection remains in the early stages of exploration. Here, we report that\n                      <jats:italic toggle=\"yes\">Ct<\/jats:italic>\n                      actively suppresses ferroptosis in host cells, with maximal inhibition at 24 hours post-infection. This suppression was demonstrated through attenuated malondialdehyde production, reduced Fe\u00b2\n                      <jats:sup>+<\/jats:sup>\n                      accumulation, and preserved mitochondrial integrity. Transcriptomic analysis of\n                      <jats:italic toggle=\"yes\">Ct<\/jats:italic>\n                      -infected cells identified PARP10 as a prominently upregulated host factor. Crucially, we discovered that\n                      <jats:italic toggle=\"yes\">Ct<\/jats:italic>\n                      -induced PARP10 inhibits NF-\u03baB activation, leading to downregulation of ferroptosis-promoting genes. Disruption of the PARP10\/NF-\u03baB axis restored ferroptosis and impaired\n                      <jats:italic toggle=\"yes\">Ct<\/jats:italic>\n                      replication. Our findings unveil a non-canonical strategy wherein\n                      <jats:italic toggle=\"yes\">Ct<\/jats:italic>\n                      exploits PARP10 to repress NF-\u03baB-dependent ferroptotic defense, thereby maintaining iron\/lipid peroxide homeostasis for intracellular survival. Targeting this pathway may offer novel anti-chlamydial therapeutics.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Chlamydia trachomatis<\/jats:italic>\n                      is a widespread bacterial infection and a leading cause of preventable blindness and sexually transmitted diseases. A key to its success is its ability to survive inside our cells by disarming the body's innate defense systems. We discovered that the bacteria actively block a potent form of cell death called ferroptosis by exploiting a human protein, PARP10. This previously unknown strategy allows\n                      <jats:italic toggle=\"yes\">Chlamydia<\/jats:italic>\n                      to create a safe haven for its replication. Uncovering this novel bacterial survival mechanism not only deepens our understanding of the infection process but also reveals the PARP10 pathway as a promising new target for developing much-needed therapeutic drugs against this pervasive pathogen.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/spectrum.03568-25","type":"journal-article","created":{"date-parts":[[2026,5,21]],"date-time":"2026-05-21T13:34:15Z","timestamp":1779370455000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["<i>Chlamydia trachomatis<\/i>\n                    inhibits NF-\u03baB-dependent ferroptosis through PARP10 upregulation to promote 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