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Chronic infections of the fallopian tubes with  Chlamydia trachomatis  ( Ctr ) cause scarring and can lead to infertility. Here we use human fallopian tube organoids and genital  Ctr  serovars D, K and E for long-term in vitro analysis. The epithelial monolayer responds with active expulsion of the bacteria into the lumen and with compensatory cellular proliferation—demonstrating a role of epithelial homeostasis in the defense against this pathogen. In addition,  Ctr  infection activates LIF signaling, which we find to be an essential regulator of stemness in the organoids. Infected organoids exhibit a less differentiated phenotype with higher stemness potential, as confirmed by increased organoid forming efficiency. Moreover,  Ctr  increases hypermethylation of DNA, which is an indicator of accelerated molecular aging. Thus, the chronic organoid infection model suggests that  Ctr  has a long-term impact on the epithelium. These heritable changes might be a contributing factor in the development of tubal pathologies, including the initiation of high grade serous ovarian cancer.

Chronic Chlamydia infection in human organoids increases stemness and promotes age-dependent CpG methylation