Placenta · 2025
NLRP3 inflammasome activation in the placenta during SARS-CoV-2 infection.
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Arboleda-Borrero Ana María, Jiménez-Charris Eliécer, Gómez Laura Andrea, Saldarriaga Wilmar, Fonseca Javier, Mosquera Escudero Mildrey
Аннотация
BACKGROUND: The NLRP3 inflammasome is a key regulator of innate immunity. Its overactivation contributes to cytokine release and tissue inflammation during SARS-CoV-2 infection. However, its role in placental inflammation and pregnancy outcomes remains unclear.
OBJECTIVE: To evaluate whether SARS-CoV-2 infection during pregnancy induces NLRP3 inflammasome activation in placental tissue and to assess its association with maternal and neonatal outcomes.
METHODS: A prospective cohort study included 25 pregnant women with RT-PCR-confirmed COVID-19 and 25 healthy controls. Placental NLRP3, Caspase-1, IL-1β, and IL-18 expression were analyzed by qRT-PCR and Western blotting. Maternal and cord plasma cytokines were quantified by ELISA and cytometric bead array. Viral RNA, antibody transfer, and nutrient transporter gene expression were also evaluated.
RESULTS: Placentas from infected women showed higher NLRP3 (p = 0.015) and Caspase-1 (p = 0.029) mRNA levels compared with controls. Western blotting detected procaspase-1 (∼50 kDa) and cleaved caspase-1 (∼35 kDa), indicating inflammasome activation. Maternal IL-18 concentrations were elevated (p = 0.013), while IL-1β remained unchanged. SARS-CoV-2 RNA was identified in 8 % of placentas (variants 21H and 20A). IgG antibodies were found in 28 % of maternal and 24 % of cord samples (p = 0.017). Infected pregnancies showed lower gestational age at delivery (p = 0.023), higher cesarean rate (p = 0.004), and lower neonatal Apgar scores (p = 0.006, p = 0.015). Nutrient transporter expression was preserved.
CONCLUSION: SARS-CoV-2 infection during pregnancy induces activation of the NLRP3 inflammasome in placental tissue and systemic elevation of IL-18, indicating both local and systemic inflammation.
OBJECTIVE: To evaluate whether SARS-CoV-2 infection during pregnancy induces NLRP3 inflammasome activation in placental tissue and to assess its association with maternal and neonatal outcomes.
METHODS: A prospective cohort study included 25 pregnant women with RT-PCR-confirmed COVID-19 and 25 healthy controls. Placental NLRP3, Caspase-1, IL-1β, and IL-18 expression were analyzed by qRT-PCR and Western blotting. Maternal and cord plasma cytokines were quantified by ELISA and cytometric bead array. Viral RNA, antibody transfer, and nutrient transporter gene expression were also evaluated.
RESULTS: Placentas from infected women showed higher NLRP3 (p = 0.015) and Caspase-1 (p = 0.029) mRNA levels compared with controls. Western blotting detected procaspase-1 (∼50 kDa) and cleaved caspase-1 (∼35 kDa), indicating inflammasome activation. Maternal IL-18 concentrations were elevated (p = 0.013), while IL-1β remained unchanged. SARS-CoV-2 RNA was identified in 8 % of placentas (variants 21H and 20A). IgG antibodies were found in 28 % of maternal and 24 % of cord samples (p = 0.017). Infected pregnancies showed lower gestational age at delivery (p = 0.023), higher cesarean rate (p = 0.004), and lower neonatal Apgar scores (p = 0.006, p = 0.015). Nutrient transporter expression was preserved.
CONCLUSION: SARS-CoV-2 infection during pregnancy induces activation of the NLRP3 inflammasome in placental tissue and systemic elevation of IL-18, indicating both local and systemic inflammation.