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<p>Congenital syphilis, a severe maternal–fetal disease caused by vertical transmission of <i>Treponema pallidum</i> (<i>T. pallidum</i>) via the placenta, affects over one million pregnancies annually and remains a leading cause of preventable adverse fetal outcomes. While the clinical consequences are well recognized, the molecular mechanisms underlying placental penetration are incompletely understood. This review synthesizes current evidence into a unified conceptual framework known as the adhesion-degradation-immune evasion cascade. Established findings, supported by direct placental studies, indicate that <i>T. pallidum</i> adhesins, including Tp0751 and Tp0136, bind trophoblast extracellular matrix receptors, while secreted enzymes such as hyaluronidase and the metalloproteinase Tp0751 degrade basement membrane components. Critically, several proposed mechanisms, including trophoblast cytoskeletal reprogramming and endocytosis, exploitation of maternal–fetal immune tolerance checkpoints (PD-L1/IDO), and modulation of Hofbauer cell polarization, await placental validation and are currently extrapolated from endothelial models, non-placental tissues, or related pathogens. This conceptual model provides a rigorous theoretical foundation for developing targeted interventions, including adhesion-blocking strategies and immune-modulatory approaches, to reduce the global burden of congenital syphilis.</p>

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Stepwise breach of maternal–fetal fortress: an adhesion-degradation-immune evasion cascade underpinning Treponema pallidum placental crossing

  • 期刊论文

  • 发表日期：

    2026年7月31日

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  • Guang Liu,
  • Zhichao Deng,
  • Hong Huang,
  • Bei Zhou,
  • Yaqi Wang,
  • Jin Lin,
  • Yanan Niu,
  • Jiaxin Chen,
  • Yanan Wei,
  • Tie Zhao,
  • Weidong Gong,
  • Yujun Tang

摘要

Congenital syphilis, a severe maternal–fetal disease caused by vertical transmission of Treponema pallidum (T. pallidum) via the placenta, affects over one million pregnancies annually and remains a leading cause of preventable adverse fetal outcomes. While the clinical consequences are well recognized, the molecular mechanisms underlying placental penetration are incompletely understood. This review synthesizes current evidence into a unified conceptual framework known as the adhesion-degradation-immune evasion cascade. Established findings, supported by direct placental studies, indicate that T. pallidum adhesins, including Tp0751 and Tp0136, bind trophoblast extracellular matrix receptors, while secreted enzymes such as hyaluronidase and the metalloproteinase Tp0751 degrade basement membrane components. Critically, several proposed mechanisms, including trophoblast cytoskeletal reprogramming and endocytosis, exploitation of maternal–fetal immune tolerance checkpoints (PD-L1/IDO), and modulation of Hofbauer cell polarization, await placental validation and are currently extrapolated from endothelial models, non-placental tissues, or related pathogens. This conceptual model provides a rigorous theoretical foundation for developing targeted interventions, including adhesion-blocking strategies and immune-modulatory approaches, to reduce the global burden of congenital syphilis.