Hormonal imbalance-mediated immune inflammation in endometrial decidualization disorder

Jiaxin Yu, Rongyan Qin, Pinxiu Huang, F Hang, Fu Hang, Yuying Guo, Yanhui Li, Yuhua Yang, Yuni Yang, Huanhuan Wu, Ying Liu, Ming Liao, Aiping Qin
Placenta · 2025 · vol. 180 , pp. 111–117 · doi:10.1016/j.placenta.2025.06.025 · PMID:40628562 · W4411919056
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This paper investigates how hormonal imbalances contribute to immune inflammation in disorders of endometrial decidualization.

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Abstract

The dynamic interplay between hormonal signalling and immune-inflammatory homeostasis is pivotal for regulating endometrial decidualization, which is indispensable for successful embryo implantation. Hormonal imbalance-mediated inflammation, particularly the imbalance between oestrogen and progesterone levels, severely disrupts endometrial decidualization. Endometriosis is characterised by oestrogen-progesterone imbalance, which is common in endometrial decidualization disorders. In endometriosis, oestrogen dominance and progesterone resistance disrupt homeostasis through multifaceted pathological mechanisms. Excessive oestrogen activates nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling, driving overproduction of pro-inflammatory cytokines and transcriptional suppression of progesterone receptor B (PR-B), thereby impairing stromal cell differentiation. Concurrent progesterone resistance attenuates anti-inflammatory responses, including NF-κB inhibition and interleukin 10 induction, and exacerbates endometrial immune dysregulation. Retinoic acid synthesis impairment and oestrogen-prostaglandin E2 feedback loops sustain a pathological hyperoestrogenic microenvironment, fostering a self-perpetuating cycle of "oestrogen dominance-inflammation-progesterone resistance". Immune disturbances at the maternal-foetal interface, such as classically activated macrophage polarisation, T-helper cell bias, and dysregulated natural killer cell cytotoxicity, further disrupt decidualization by impairing immunotolerance. Therefore, therapeutic strategies targeting these pathways are promising. Dienogest suppresses aromatase/cyclooxygenase-2 (COX-2)-mediated oestrogen synthesis and restores progesterone sensitivity via PR-B upregulation. Immunomodulatory approaches, including corticosteroids and tumour necrosis factor-α inhibitors, improve pregnancy outcomes in endometriosis-associated infertility. Future research, leveraging state-of-the-art technologies, should prioritise elucidating the molecular interactions within the oestrogen-progesterone-immune axis and translating these insights into personalised therapies to optimise the management of decidualization-related disorders.

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MeSH descriptors

Decidua Decidua Decidua Decidua Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Endometrium Estrogens Estrogens Inflammation Inflammation Inflammation Progesterone Progesterone Animals Embryo Implantation

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