Abstract
The hypothalamus–pituitary–adrenal (HPA) axis was described as the principal component of the stress response 85 years ago, along with the acute-phase reaction, and the defense response at the tissue level. The orchestration of these processes is essential since systemic inflammation is a double-edged sword; whereas inflammation that is timely and of appropriate magnitude is beneficial, exuberant systemic inflammation incites tissue damage with potentially devastating consequences. Apart from its beneficial cardiovascular and metabolic effects, cortisol exerts a significant immunoregulatory role, a major attribute being that it restrains the excessive inflammatory reaction, thereby preventing unwanted tissue damage. In this review, we will discuss the role of the HPA axis in the normal stress response and in critical illness, especially in critically ill patients with coronavirus disease 2019 (COVID-19). Finally, a chapter will be dedicated to the findings from clinical studies in critical illness and COVID-19 on the expression of the mediator of glucocorticoid actions, the glucocorticoid receptor (GCR).
Highlights
The activation of the hypothalamus–pituitary–adrenal (HPA) axis is a principal component of the stress response evoked by systemic inflammation [1], and occurs in conjunction with the acute-phase reaction and the tissue level defense process
Apart from its beneficial cardiovascular and metabolic effects, excess cortisol originating by HPA axis activation exerts significant immunoregulatory effects [4], with a major attribute being that it restrains the excessive inflammatory reaction, thereby preventing unwanted tissue damage
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of coronavirus disease 2019 (COVID-19), a disease with a wide range of clinical manifestations; most infected subjects remain asymptomatic or with a mild disease, a number develop a respiratory illness of variable severity that, in some cases, can progress to acute respiratory distress syndrome (ARDS), multi-organ failure, and death
Summary
The activation of the hypothalamus–pituitary–adrenal (HPA) axis is a principal component of the stress response evoked by systemic inflammation [1], and occurs in conjunction with the acute-phase reaction and the tissue level defense process. Sympathetic preganglionic fibers (whose trunks rest on the lower thoracic and upper lumbar spine) and parasympathetic fibers from the abdominal branch of the pneumogastric nerve form networks that penetrate the adrenal cortex passing into the medulla. This design can play a role in regulating adrenal cortical function during stressful situations, providing a neural pathway that connects the adrenal glands to the hypothalamus [6]
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