[Advances in the role of adrenal microenvironment in maintaining homeostasis under inflammatory stress]

Sepsis is one of the major diseases threatening human health. Under inflammatory stress, the rapid activation of glucocorticoids (GCs) and catecholamines (CAs) in the adrenal gland is crucial for maintaining the body's homeostasis. During severe inflammation, impairment of the hypothalamic-pituitary-adrenal (HPA) axis leads to suppressed secretion of corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACHT). However, studies reveal that the systemic glucocorticoid levels can remain normal or even elevated, suggesting a transition in the stress response mechanism from the central, pituitary-dependent regulatory system to local, pituitary-independent regulatory mechanisms. Among the various potential mechanisms, activation of the local adrenal microenvironment plays a significant role. In this microenvironment, interactions between adrenal cortical cells, medullary cells, vascular endothelial cells, and various immune cells contribute to the sustained production of GCs, which is pivotal in maintaining the internal homeostasis. This review focuses on the role of the local adrenal microenvironment in regulating the secretion of GCs and CAs, key hormones for maintaining homeostasis under inflammatory stress, with the aim of providing new insights into the etiology and pathogenesis of adrenal diseases.