ArticleFrontiers in immunology2023
Di(2-ethylhexyl) phthalate mediates IL-33 production
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The impact of Di(2-ethylhexyl) phthalate on human organ development: mechanisms and clinical relevance review.Frontiers in public health · 2026Review
- Yangke powder alleviates OVA-induced allergic asthma by inhibiting the PI3K/AKT/NF-κB signaling pathway.Chinese medicine · 2025Article
- Association of Phthalate Exposure with Respiratory and Allergic Symptoms and Type 2 and Non-Type 2 Inflammation: The Hokkaido Study.Environmental science & technology · 2025Article
- Dietary exposure to di(2-ethylhexyl) phthalate for 6 months alters markers of female reproductive aging in mice†.Biology of reproduction · 2025Article
- Phthalates and epigenetics: An emerging public health concern.Current research in toxicology · 2025Review
- The role of the aryl hydrocarbon receptor in mediating the effects of mono(2-ethylhexyl) phthalate in mouse ovarian antral follicles†.Biology of reproduction · 2024Article
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Authors and funding
10 authors.
Funding
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Abstract
Background: Few studies assess cord blood biomarkers to predict prenatal exposure to di(2-ethylhexyl) phthalate (DEHP) on the development of allergic diseases later in childhood. IL-33 has been indicated to play an important role in allergic diseases. We evaluated the association of prenatal DEHP exposure and IL-33 in cord blood on the development of allergic diseases. We also investigated the mechanism of DEHP in human lung epithelial cells and asthma animal models. Methods: 66 pregnant women were recruited, and their children followed when they were aged 3 years. Maternal urinary DEHP metabolites were determined using liquid chromatography-electrospray-ionization-tandem mass spectrometry. The effect of DEHP on IL-33 production was investigated in human lung epithelial cells and club cell-specific aryl hydrocarbon receptor (AhR) deficiency mice. ELISA and RT-PCR, respectively, measured the IL-33 cytokine concentration and mRNA expression. Results: The concentrations of maternal urinary DEHP metabolites and serum IL-33 in cord blood with childhood allergy were significantly higher than those in the non-childhood allergy group. DEHP and MEHP could induce IL-33 production and reverse by AhR antagonist and flavonoids Conclusions: Cord blood IL-33 level was correlated to childhood allergy and associated with maternal DEHP exposure. IL-33 might be a potential target to assess the development of DEHP-related childhood allergic disease. Flavonoids might be the natural antidotes for DEHP.
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