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REVIEW article
Front. Endocrinol.
Sec. Molecular and Structural Endocrinology
Volume 16 - 2025 | doi: 10.3389/fendo.2025.1448750
This article is part of the Research Topic Linking the Endocrine System With Immunity View all 8 articles
Corticosterone effects induced by stress and immunity and inflammation: mechanisms of communication
Provisionally accepted- 1 College of Traditional Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China
- 2 Department of Endocrinology, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Nankai District, Tianjin, China
The body instinctively responds to external stimuli by increasing energy metabolism and initiating immune responses upon receiving stress signals. Corticosterone (CORT), a glucocorticoid (GC) that regulates secretion along the hypothalamic-pituitary-adrenal (HPA) axis, mediates neurotransmission and humoral regulation. Due to the widespread expression of glucocorticoid receptors (GR), the effects of CORT are almost ubiquitous in various tissue cells. Therefore, on the one hand, CORT is a molecular signal that activates the body's immune system during stress and on the other hand, due to the chemical properties of GCs, the anti-inflammatory properties of CORT act as stabilizers to control the body's response to stress. Inflammation is a manifestation of immune activation. CORT plays dual roles in this process by both promoting inflammation and exerting anti-inflammatory effects in immune regulation. As a stress hormone, CORT levels fluctuate with the degree and duration of stress, determining its effects and the immune changes it induces. The immune system is essential for the body to resist diseases and maintain homeostasis, with immune imbalance being a key factor in the development of various diseases. Therefore, understanding the role of CORT and its mechanisms of action on immunity is crucial. This review addresses this important issue and summarizes the interactions between CORT and the immune system.
Keywords: stress, Corticosterone, Immunity, Inflammation, mechanism feedback signal transmission/activation. -: Negative feedback signal transmission/suppression
Received: 14 Aug 2024; Accepted: 28 Feb 2025.
Copyright: © 2025 Xu, Wang and Haiqing. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Jingyu Xu, College of Traditional Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China
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