Cutaneous Glucocorticoidogenesis and Cortisol Signaling Are Defective in Psoriasis

Andrzej T Slominski; Anna A Brożyna; Robert C Tuckey

doi:10.1016/j.jid.2017.04.004

Cutaneous Glucocorticoidogenesis and Cortisol Signaling Are Defective in Psoriasis

J Invest Dermatol. 2017 Aug;137(8):1609-1611. doi: 10.1016/j.jid.2017.04.004.

Authors

Andrzej T Slominski¹, Anna A Brożyna², Robert C Tuckey³

Affiliations

¹ Department of Dermatology, University of Alabama at Birmingham, Birmingham, Alabama, USA; Comprehensive Cancer Center, Cancer Chemoprevention Program, University of Alabama at Birmingham, Birmingham, Alabama, USA; Nutrition Obesity Research Center, University of Alabama at Birmingham, Birmingham, Alabama, USA; VA Medical Center, Birmingham, Alabama, USA. Electronic address: aslominski@uabmc.edu.
² Department of Dermatology, University of Alabama at Birmingham, Birmingham, Alabama, USA; Department of Tumor Pathology and Pathomorphology, Oncology Centre-Prof. Franciszek Łukaszczyk Memorial Hospital, Bydgoszcz, Poland; Department of Tumor Pathology and Pathomorphology, Faculty of Health Sciences, Nicolaus Copernicus University Collegium Medicum in Bydgoszcz, Bydgoszcz, Poland.
³ School of Molecular Sciences, The University of Western Australia, Perth, WA, Australia.

Abstract

Hannen et al. report that cutaneous glucocorticoidogenesis and expression of glucocorticoid receptors are inhibited in psoriatic skin. These findings substantiate the previous concept that deficient feedback of local proopiomelanocortin and glucocorticoids on cutaneous immunity contributes to inflammatory and autoimmune dermatoses. Restoration of efficient endogenous glucocorticoid signaling represents a realistic goal in treating psoriasis.

Publication types

Review
Research Support, N.I.H., Extramural
Comment

MeSH terms

Administration, Cutaneous
Anti-Inflammatory Agents / administration & dosage
Anti-Inflammatory Agents / pharmacokinetics
Humans
Hydrocortisone / administration & dosage
Hydrocortisone / pharmacokinetics*
Psoriasis* / drug therapy
Psoriasis* / metabolism
Psoriasis* / pathology
Receptors, Glucocorticoid / metabolism*
Signal Transduction
Skin / drug effects
Skin / metabolism*
Skin / pathology

Substances

Anti-Inflammatory Agents
Receptors, Glucocorticoid
Hydrocortisone

Abstract

Publication types

MeSH terms

Substances

Grants and funding