Cause or consequence? Understanding the role of cortisol in the increased inflammation observed in depression

Nare Amasi-Hartoonian; Luca Sforzini; Annamaria Cattaneo; Carmine Maria Pariante

doi:10.1016/j.coemr.2022.100356

Cause or consequence? Understanding the role of cortisol in the increased inflammation observed in depression

Nare Amasi-Hartoonian^*, Luca Sforzini, Annamaria Cattaneo, Carmine Maria Pariante

^*Corresponding author for this work

Research output: Contribution to journal › Review article › peer-review

19 Citations (Scopus)

Abstract

Glucocorticoids such as cortisol are a class of steroid hormones that play an important role in co-ordinating the body's response to stress. Elevated cortisol levels and increased inflammation have frequently been reported in patients with depression. The currently accepted ‘glucocorticoid resistance’ model posits this increased inflammation as a consequence of reduced sensitivity to cortisol's putative anti-inflammatory action. However, opposing evidence has accumulated that supports a more recent model, which instead proposes that cortisol possesses immune potentiating properties and may thus directly cause the increased inflammation seen in depression. Despite all of this, a clear explanation of the neuroendocrine mechanism that contributes to the development of depression is still lacking and thus requires further investigation in improved future studies.

Original language	English
Article number	100356
Journal	Current Opinion in Endocrine and Metabolic Research
Volume	24
DOIs	https://doi.org/10.1016/j.coemr.2022.100356
Publication status	Published - Jun 2022

Keywords

Cortisol
Glucocorticoid receptor
Glucocorticoid resistance
Hypothalamic-pituitary-adrenal axis
Inflammation
Major depressive disorder

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/j.coemr.2022.100356

Cite this

@article{fa9cd290b4e24c46b36dd47230b23110,

title = "Cause or consequence? Understanding the role of cortisol in the increased inflammation observed in depression",

abstract = "Glucocorticoids such as cortisol are a class of steroid hormones that play an important role in co-ordinating the body's response to stress. Elevated cortisol levels and increased inflammation have frequently been reported in patients with depression. The currently accepted {\textquoteleft}glucocorticoid resistance{\textquoteright} model posits this increased inflammation as a consequence of reduced sensitivity to cortisol's putative anti-inflammatory action. However, opposing evidence has accumulated that supports a more recent model, which instead proposes that cortisol possesses immune potentiating properties and may thus directly cause the increased inflammation seen in depression. Despite all of this, a clear explanation of the neuroendocrine mechanism that contributes to the development of depression is still lacking and thus requires further investigation in improved future studies.",

keywords = "Cortisol, Glucocorticoid receptor, Glucocorticoid resistance, Hypothalamic-pituitary-adrenal axis, Inflammation, Major depressive disorder",

author = "Nare Amasi-Hartoonian and Luca Sforzini and Annamaria Cattaneo and Pariante, {Carmine Maria}",

note = "Funding Information: Research funded by the National Institute for Health Research (NIHR) Maudsley Biomedical Research Centre (BRC) , London, United Kingdom. This work was also supported by the Wellcome Trust strategy award to the Neuroimmunology of Mood Disorders and Alzheimer's Disease (NIMA) Consortium (104025), which is also funded by Janssen, GlaxoSmithKline, Lundbeck and Pfizer. Funding Information: The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:, Research funded by the National Institute for Health Research (NIHR) Maudsley Biomedical Research Centre (BRC), London, United Kingdom. This work was also supported by the Wellcome Trust strategy award to the Neuroimmunology of Mood Disorders and Alzheimer's Disease (NIMA) Consortium (104025), which is also funded by Janssen, GlaxoSmithKline, Lundbeck and Pfizer. Dr. Sforzini and Prof. Pariante have received research funding from the Innovative Medicines Initiative 2 Joint Undertaking under grant agreement No 853966–2, as part of the EU-PEARL project. This Joint Undertaking receives support from the European Union's Horizon 2020 research and innovation programme and EFPIA. Prof. Pariante has also received research funding from Johnson & Johnson as part of a program of research on depression and inflammation and speakers and consultation fees from Lundbeck and Boehringer Ingelheim. Funding Information: Dr. Sforzini and Prof. Pariante have received research funding from the Innovative Medicines Initiative 2 Joint Undertaking under grant agreement No 853966–2 , as part of the EU-PEARL project. This Joint Undertaking receives support from the European Union{\textquoteright}s Horizon 2020 research and innovation programme and EFPIA . Prof. Pariante has also received research funding from Johnson & Johnson as part of a program of research on depression and inflammation and speakers and consultation fees from Lundbeck and Boehringer Ingelheim. Publisher Copyright: {\textcopyright} 2022 The Authors",

year = "2022",

month = jun,

doi = "10.1016/j.coemr.2022.100356",

language = "English",

volume = "24",

journal = "Current Opinion in Endocrine and Metabolic Research",

issn = "2451-9650",

publisher = "Elsevier Ltd",

}

TY - JOUR

T1 - Cause or consequence? Understanding the role of cortisol in the increased inflammation observed in depression

AU - Amasi-Hartoonian, Nare

AU - Sforzini, Luca

AU - Cattaneo, Annamaria

AU - Pariante, Carmine Maria

N1 - Funding Information: Research funded by the National Institute for Health Research (NIHR) Maudsley Biomedical Research Centre (BRC) , London, United Kingdom. This work was also supported by the Wellcome Trust strategy award to the Neuroimmunology of Mood Disorders and Alzheimer's Disease (NIMA) Consortium (104025), which is also funded by Janssen, GlaxoSmithKline, Lundbeck and Pfizer. Funding Information: The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:, Research funded by the National Institute for Health Research (NIHR) Maudsley Biomedical Research Centre (BRC), London, United Kingdom. This work was also supported by the Wellcome Trust strategy award to the Neuroimmunology of Mood Disorders and Alzheimer's Disease (NIMA) Consortium (104025), which is also funded by Janssen, GlaxoSmithKline, Lundbeck and Pfizer. Dr. Sforzini and Prof. Pariante have received research funding from the Innovative Medicines Initiative 2 Joint Undertaking under grant agreement No 853966–2, as part of the EU-PEARL project. This Joint Undertaking receives support from the European Union's Horizon 2020 research and innovation programme and EFPIA. Prof. Pariante has also received research funding from Johnson & Johnson as part of a program of research on depression and inflammation and speakers and consultation fees from Lundbeck and Boehringer Ingelheim. Funding Information: Dr. Sforzini and Prof. Pariante have received research funding from the Innovative Medicines Initiative 2 Joint Undertaking under grant agreement No 853966–2 , as part of the EU-PEARL project. This Joint Undertaking receives support from the European Union’s Horizon 2020 research and innovation programme and EFPIA . Prof. Pariante has also received research funding from Johnson & Johnson as part of a program of research on depression and inflammation and speakers and consultation fees from Lundbeck and Boehringer Ingelheim. Publisher Copyright: © 2022 The Authors

PY - 2022/6

Y1 - 2022/6

N2 - Glucocorticoids such as cortisol are a class of steroid hormones that play an important role in co-ordinating the body's response to stress. Elevated cortisol levels and increased inflammation have frequently been reported in patients with depression. The currently accepted ‘glucocorticoid resistance’ model posits this increased inflammation as a consequence of reduced sensitivity to cortisol's putative anti-inflammatory action. However, opposing evidence has accumulated that supports a more recent model, which instead proposes that cortisol possesses immune potentiating properties and may thus directly cause the increased inflammation seen in depression. Despite all of this, a clear explanation of the neuroendocrine mechanism that contributes to the development of depression is still lacking and thus requires further investigation in improved future studies.

AB - Glucocorticoids such as cortisol are a class of steroid hormones that play an important role in co-ordinating the body's response to stress. Elevated cortisol levels and increased inflammation have frequently been reported in patients with depression. The currently accepted ‘glucocorticoid resistance’ model posits this increased inflammation as a consequence of reduced sensitivity to cortisol's putative anti-inflammatory action. However, opposing evidence has accumulated that supports a more recent model, which instead proposes that cortisol possesses immune potentiating properties and may thus directly cause the increased inflammation seen in depression. Despite all of this, a clear explanation of the neuroendocrine mechanism that contributes to the development of depression is still lacking and thus requires further investigation in improved future studies.

KW - Cortisol

KW - Glucocorticoid receptor

KW - Glucocorticoid resistance

KW - Hypothalamic-pituitary-adrenal axis

KW - Inflammation

KW - Major depressive disorder

UR - http://www.scopus.com/inward/record.url?scp=85131075734&partnerID=8YFLogxK

U2 - 10.1016/j.coemr.2022.100356

DO - 10.1016/j.coemr.2022.100356

M3 - Review article

AN - SCOPUS:85131075734

SN - 2451-9650

VL - 24

JO - Current Opinion in Endocrine and Metabolic Research

JF - Current Opinion in Endocrine and Metabolic Research

M1 - 100356

ER -

Cause or consequence? Understanding the role of cortisol in the increased inflammation observed in depression

Abstract

Keywords

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this