Cytokines and inflammatory mediators in amniotic fluid as predictive markers of congenital infections.

Fiche publication

Date publication

février 2026

Journal

European journal of obstetrics, gynecology, and reproductive biology

Auteurs

Membres identifiés du Cancéropôle Est :
Pr VILLENA Isabelle

Tous les auteurs :
Ameyoud B, Manier A, Escotte S, Bory JP, Greigert V, Villena I

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/41722347

Résumé

During pregnancy, a finely regulated balance between inflammatory and regulatory immune responses supports maternal-fetal tolerance while preserving defense against pathogens. Various congenital infections can disrupt this equilibrium and impair fetal development. Amniotic fluid plays a central role in fetal protection, particularly through its cytokine composition, which mirrors the immune status during pregnancy. In the context of congenital infection (bacterial, viral, or parasitic), the cytokine profile is altered, thereby influencing fetal prognosis. Numerous studies have examined the impact of congenital infections on the immune response and their consequences for both mother and fetus. However, data on the inflammatory profile of amniotic fluid remain limited, owing to the invasiveness of sampling procedures and the complexity of analyses. A deeper understanding of inflammatory changes in amniotic fluid would provide valuable insights into the pathogenesis of fetal diseases, facilitate the identification of predictive biomarkers for congenital lesions, and contribute to the development of new therapeutic strategies. This article provides an update on the pathophysiology of infections with congenital transmission, focusing on the immune response to bacteria, viruses, and parasites. Particular attention is given to congenital toxoplasmosis. Results and conclusions : data on the cytokine profile in amniotic fluid are limited. The cytokine profile varies depending on the type of pathogen. For Toxoplasma gondii, data are difficult to interpret but the cytokine profile to acute infection is strain-dependent.