Placental leukocyte infiltration accompanies gestational changes induced by hyperthyroidism

Area of Science:

• Endocrinology
• Immunology
• Reproductive Biology

Background:

• Thyroid dysfunctions cause reproductive complications by altering the maternal-fetal interface.
• Thyroid hormones (THs) regulate immune cells and cytokine expression, but their role in placental immunology during hyperthyroidism is unclear.

Purpose of the Study:

• To investigate how hyperthyroidism modulates placental immunological and morphological aspects.
• To elucidate the impact of thyroid hormones on immune cell activation and placental development.

Main Methods:

• Wistar rats with induced hyperthyroidism were mated and euthanized at specific pregnancy stages (G19, G20).
• Placental tissues underwent qPCR, flow cytometry, immunohistochemistry, Western blot, and histological analysis.
• Hormone levels in amniotic fluid and serum were evaluated; in vitro assays assessed immune cell activation.

Main Results:

• Hyperthyroidism increased fetal and placental weight, altered placental morphology (basal zone, decidua), and induced endocrine imbalance (higher corticosterone).
• Increased mRNA expression of glucocorticoid receptor and monocyte chemoattractant protein-1, and prolactin receptor (mRNA and protein) were observed.
• Increased CD45+ immune cell infiltration and TH-induced immune cell activation were evidenced.

Conclusions:

• Hyperthyroidism significantly modulates placental immunological and morphological features.
• These placental changes induced by thyroid hormones may contribute to altered fetal development and preterm labor observed in hyperthyroid pregnancies.