Pathogenesis of preterm birth: bidirectional inflammation in mother and fetus

Area of Science:

• Immunology
• Reproductive Biology
• Maternal-Fetal Medicine

Background:

• Preterm birth (PTB) affects 5-18% of global pregnancies, causing significant maternal and fetal morbidity/mortality.
• The causes of spontaneous PTB are largely unknown, hindering effective prediction and prevention.
• Maternal immune adaptations are critical for successful pregnancy, and their dysfunction is linked to PTB.

Purpose of the Study:

• To review current knowledge on fetal-maternal communication in the context of PTB.
• To explore the role of immune dysregulation in the immunopathogenesis of PTB.
• To highlight insights advancing the understanding of PTB pathogenesis.

Main Methods:

• Review of existing literature, including human studies and animal models (primarily mouse models).
• Examination of evidence on maternal immune adaptations and fetal-maternal tolerance.
• Analysis of bidirectional communication between fetal and maternal systems.

Main Results:

• Evidence supports PTB results from a breakdown in fetal-maternal tolerance.
• Excessive and premature inflammation plays a significant role in PTB pathogenesis.
• Mouse models and human studies provide insights into immune dysfunctions contributing to PTB.

Conclusions:

• Bidirectional fetal-maternal communication is crucial in the immunopathogenesis of PTB.
• Understanding these interactions advances knowledge of PTB pathogenesis.
• These insights are essential for developing effective PTB prediction and prevention strategies.