Systematic low-grade chronic inflammation and intrinsic mechanisms in polycystic ovary syndrome

Front Immunol. 2024 Dec 19:15:1470283. doi: 10.3389/fimmu.2024.1470283. eCollection 2024.

Abstract

Polycystic ovary syndrome (PCOS) is a prevalent endocrine and metabolic disorder affecting 6-20% of women of childbearing age worldwide. Immune cell imbalance and dysregulation of inflammatory factors can lead to systematic low-grade chronic inflammation (SLCI), which plays a pivotal role in the pathogenesis of PCOS. A significant higher infiltration of immune cells such as macrophages and lymphocytes and pro-inflammatory factors IL-6 and TNF-α has been detected in PCOS organ systems, impacting not only the female reproductive system but also other organs such as the cardiovascular, intestine, liver, thyroid, brain and other organs. Obesity, insulin resistance (IR), steroid hormones imbalance and intestinal microecological imbalance, deficiencies in vitamin D and selenium, as well as hyperhomocysteinemia (HHcy) can induce systematic imbalance between pro-inflammatory and anti-inflammatory cells and molecules. The pro-inflammatory cells and cytokines also interact with obesity, steroid hormones imbalance and IR, leading to increased metabolic imbalance and reproductive-endocrine dysfunction in PCOS patients. This review aims to summarize the dysregulation of immune response in PCOS organ system and the intrinsic mechanisms affecting SLCI in PCOS to provide new insights for the systemic inflammatory treatment of PCOS in the future.

Keywords: chronic inflammation; intestinal microecological; intrinsic mechanisms; polycystic ovary syndrome; steroid hormones.

Publication types

  • Review

MeSH terms

  • Animals
  • Chronic Disease
  • Cytokines / metabolism
  • Female
  • Humans
  • Inflammation Mediators / metabolism
  • Inflammation* / immunology
  • Insulin Resistance / immunology
  • Obesity / immunology
  • Obesity / metabolism
  • Polycystic Ovary Syndrome* / immunology
  • Polycystic Ovary Syndrome* / metabolism

Substances

  • Cytokines
  • Inflammation Mediators

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. The research was supported by the General Project of Natural science foundation project of Sichuan (2024NSFSC0599, 2023NSFSC0632), the Key Research and Development Program of Chengdu (2023-YF09-00052-SN), the Key Program of Development Fund for Clinical Disciplines of West China Second Hospital of Sichuan University (KL059), the General Project of National Natural Science Foundation of China (81971354), and the health department of Sichuan province (100377).