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Related Concept Videos

Teratogenicity01:07

Teratogenicity

The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...

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Updated: Jun 16, 2026

Moderate Prenatal Alcohol Exposure and Quantification of Social Behavior in Adult Rats
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Moderate Prenatal Alcohol Exposure and Quantification of Social Behavior in Adult Rats

Published on: December 14, 2014

Gestational PFOS Exposure Induces Alveolar Developmental Defects by Affecting Immune-Epithelial Crosstalk in

Jingye Zuo1, Jiali Mo1, Shuting Weng1

  • 1Department of Pediatric Pulmonology, Children's Medical Center, Peking University First Hospital, Beijing, China.

Journal of Applied Toxicology : JAT
|June 14, 2026
PubMed
Summary
This summary is machine-generated.

Gestational exposure to Perfluorooctane sulfonate (PFOS) causes lung developmental defects in offspring, leading to bronchopulmonary dysplasia-like pathology. This occurs due to altered immune cell function and disrupted alveolar epithelial cell differentiation.

Keywords:
Sprague–Dawley ratgene expressionimmune–epithelial crosstalklung developmentperfluorooctane sulfonatesingle‐cell RNA sequencingrisk assessment

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Published on: June 24, 2020

Area of Science:

  • Environmental Toxicology
  • Developmental Biology
  • Pulmonary Medicine

Background:

  • Perfluorooctane sulfonate (PFOS) is an endocrine-disrupting compound with known adverse effects on offspring development.
  • Gestational exposure to environmental toxins can lead to long-term health consequences, particularly in developing organs like the lungs.
  • The precise cellular and molecular mechanisms by which PFOS impacts lung development remain incompletely understood.

Purpose of the Study:

  • To investigate the effects of gestational PFOS exposure on offspring lung development in a rat model.
  • To elucidate the cellular and molecular mechanisms underlying PFOS-induced pulmonary toxicity.
  • To identify key cellular players and signaling pathways involved in developmental lung defects caused by PFOS.

Main Methods:

  • Oral administration of PFOS to pregnant rats during critical developmental windows (gestational days 11-20).
  • Assessment of offspring lung pathology at multiple postnatal time points (0, 7, 14, 21 days).
  • Single-cell RNA sequencing (scRNA-seq) to analyze pulmonary cellular landscape and gene expression.
  • Intercellular communication analysis to predict signaling pathways.

Main Results:

  • Gestational PFOS exposure induced bronchopulmonary dysplasia (BPD)-like pathology, including simplified alveoli, glycogen retention, and collagen deposition.
  • scRNA-seq revealed significant remodeling of lung cell populations, characterized by accumulation of transitional alveolar epithelial type II cells (AECIIs).
  • Alveolar macrophages shifted towards pro-inflammatory and pro-fibrotic phenotypes, with evidence suggesting the FN1-CD44 axis as a key mediator of epithelial defects via immune-epithelial crosstalk.

Conclusions:

  • Disruption of AECII differentiation is a critical event in PFOS-induced alveolar developmental defects.
  • Immune-epithelial cell communication plays a significant role in the pulmonary toxicity mediated by PFOS.
  • These findings provide novel insights into the mechanisms of environmental endocrine disruptors on lung development.