Related Experiment Video
Updated: Jan 2, 2026
Modeling Ascending Vaginal Infection, Preterm Birth, and Neonatal Morbidity in Mice
Published on: October 10, 2025
Association of modulation of pro-inflammatory responses by dectin-2 with preterm delivery: An experimental model
Aspasia Liassidou1, Georgios Renieris1, Dionysia-Irene Droggiti1
14th Department of Internal Medicine, Medical School, National and Kapodistrian University of Athens, Athens, Greece.
Problem:
Pro-inflammatory responses of pathogen recognition receptors (PRR) are implicated in preterm delivery (PTD). Dectin-2 is one PRR recognizing unselective carbohydrate structures; its participation in PTD has never been studied before.
Method Of Study:
In an experimental model, PTD was induced in female pregnant wild-type (WT) mice and mice with homologous deficiency for dectin-2 by the intraperitoneal injection of bacterial lipopolysaccharide (LPS) on day 14 of pregnancy. Time to delivery and fetal mortality were recorded. Challenged mice were killed for tissue collection and splenocyte isolation 6 hours later. Concentrations of tumour necrosis factor-alpha (TNFα), interleukin (IL)-1α, and IL-1β were measured.
Results:
Delivery was induced significantly earlier in WT than dectin-2-/- mice; however, fetal mortality was higher among dectin-2-/- mice. Candida albicans challenge could not lead to these changes. Sacrifice experiments showed that LPS challenge led to significant increase of TNFα, IL-1α, and IL-1β in maternal tissues of WT; this was further enhanced for TNFα and IL-1β in dectin-2-/- mice. Pre-treatment with the prostaglandin inhibitor diclofenac delayed time to delivery of WT mice, but not of dectin2-/- mice. TNFα stimulation of splenocytes of dectin2-/- mice was enhanced with the addition of anti-TLR4 and decreased in the presence of lipid A.
Conclusions:
Dectin-2 delays LPS-induced PTD by enhancing the production of pro-inflammatory cytokines.
