Ex vivo study shows standard preterm labor medications minimally alter inflammatory markers in human placental explants, indicating that timing limits betamethasone's anti-inflammatory efficacy.
Problem Patients with threatened preterm labor (PTL) are treated with antibiotics, corticosteroids, and magnesium sulfate to mitigate infection, promote fetal lung maturation, provide fetal neuroprotection and overall minimize the impact of prematurity on the neonate. However, the effect of these drugs on the placental inflammatory profile is unknown even though these are given systemically and reach the placenta. We evaluated their action in an ex vivo model of placental inflammation. Method of Study Placental explants from uncomplicated pregnancies were exposed to lipopolysaccharide (LPS) ± azithromycin, betamethasone, and/or magnesium sulfate. Production (lysate) and secretion (supernatant) of pro‐ and anti‐inflammatory cytokines were assessed by ELISA. Results Both pro‐ and anti‐inflammatory cytokines were increased by LPS versus untreated. Azithromycin, or magnesium sulfate did not alter the inflammatory profile by themselves nor when added at the same time or 24 h after LPS. Betamethasone decreased both pro‐ and anti‐inflammatory cytokines only when administered at the same time as LPS, without any effects if delayed. Conclusions Therapeutic interventions classically used for preterm labor (PTL) do not impact the placental inflammatory profile by themselves or in the context of an ex vivo placental explants model of LPS‐induced inflammation, except for betamethasone when administered concurrently with LPS.
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Weng et al. (2026) studied this question.
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