Probing the effects of stress mediators on the human hair follicle

Substance P holds central position

Eva M.J. Peters, Sofia Liotiri, Eniko Bodó, Evelin Hagen, Tamás Bíró, Petra C. Arck, Ralf Paus

Research output: Contribution to journalArticle

105 Citations (Scopus)

Abstract

Stress alters murine hair growth, depending on substance P-mediated neurogenic inflammation and nerve growth factor (NGF), a key modulator of hair growth termination (catagen induction). Whether this is of any relevance in human hair follicles (HFs) is completely unclear. Therefore, we have investigated the effects of substance P, the central cutaneous prototypic stress-associated neuropeptide, on normal, growing human scalp HFs in organ culture. We show that these prominently expressed substance P receptor (NK1) at the gene and protein level. Organ-cultured HFs responded to substance P by premature catagen development, down-regulation of NK1, and up-regulation of neutral endopeptidase (degrades substance P). This was accompanied by mast cell degranulation in the HF connective tissue sheath, indicating neurogenic inflammation. Substance P down-regulated immunoreactivity for the growth-promoting NGF receptor (TrkA), whereas it up-regulated NGF and its apoptosis- and catagen-promoting receptor (p75NTR). In addition, MHC class I and β2-microglobulin immunoreactivity were up-regulated and detected ectopically, Indicating collapse of the HF immune privilege. In conclusion, we present a simplistic, but instructive, organ culture assay to demonstrate sensitivity of the human HF to key skin stress mediators. The data obtained therewith allow one to sketch the first evidence-based biological explanation for how stress may trigger or aggravate telogen effluvium and alopecia areata.

Original languageEnglish (US)
Pages (from-to)1872-1886
Number of pages15
JournalAmerican Journal of Pathology
Volume171
Issue number6
DOIs
StatePublished - Jan 1 2007
Externally publishedYes

Fingerprint

Hair Follicle
Substance P
Neurogenic Inflammation
Organ Culture Techniques
Nerve Growth Factor
Hair
Growth
Alopecia Areata
Neurokinin-1 Receptors
Nerve Growth Factor Receptor
Cell Degranulation
Neprilysin
Skin
Scalp
Neuropeptides
Mast Cells
Connective Tissue
Up-Regulation
Down-Regulation
Apoptosis

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Probing the effects of stress mediators on the human hair follicle : Substance P holds central position. / Peters, Eva M.J.; Liotiri, Sofia; Bodó, Eniko; Hagen, Evelin; Bíró, Tamás; Arck, Petra C.; Paus, Ralf.

In: American Journal of Pathology, Vol. 171, No. 6, 01.01.2007, p. 1872-1886.

Research output: Contribution to journalArticle

Peters, Eva M.J. ; Liotiri, Sofia ; Bodó, Eniko ; Hagen, Evelin ; Bíró, Tamás ; Arck, Petra C. ; Paus, Ralf. / Probing the effects of stress mediators on the human hair follicle : Substance P holds central position. In: American Journal of Pathology. 2007 ; Vol. 171, No. 6. pp. 1872-1886.
@article{0086e75623b34f879710a28a921dc92a,
title = "Probing the effects of stress mediators on the human hair follicle: Substance P holds central position",
abstract = "Stress alters murine hair growth, depending on substance P-mediated neurogenic inflammation and nerve growth factor (NGF), a key modulator of hair growth termination (catagen induction). Whether this is of any relevance in human hair follicles (HFs) is completely unclear. Therefore, we have investigated the effects of substance P, the central cutaneous prototypic stress-associated neuropeptide, on normal, growing human scalp HFs in organ culture. We show that these prominently expressed substance P receptor (NK1) at the gene and protein level. Organ-cultured HFs responded to substance P by premature catagen development, down-regulation of NK1, and up-regulation of neutral endopeptidase (degrades substance P). This was accompanied by mast cell degranulation in the HF connective tissue sheath, indicating neurogenic inflammation. Substance P down-regulated immunoreactivity for the growth-promoting NGF receptor (TrkA), whereas it up-regulated NGF and its apoptosis- and catagen-promoting receptor (p75NTR). In addition, MHC class I and β2-microglobulin immunoreactivity were up-regulated and detected ectopically, Indicating collapse of the HF immune privilege. In conclusion, we present a simplistic, but instructive, organ culture assay to demonstrate sensitivity of the human HF to key skin stress mediators. The data obtained therewith allow one to sketch the first evidence-based biological explanation for how stress may trigger or aggravate telogen effluvium and alopecia areata.",
author = "Peters, {Eva M.J.} and Sofia Liotiri and Eniko Bod{\'o} and Evelin Hagen and Tam{\'a}s B{\'i}r{\'o} and Arck, {Petra C.} and Ralf Paus",
year = "2007",
month = "1",
day = "1",
doi = "10.2353/ajpath.2007.061206",
language = "English (US)",
volume = "171",
pages = "1872--1886",
journal = "American Journal of Pathology",
issn = "0002-9440",
publisher = "Elsevier Inc.",
number = "6",

}

TY - JOUR

T1 - Probing the effects of stress mediators on the human hair follicle

T2 - Substance P holds central position

AU - Peters, Eva M.J.

AU - Liotiri, Sofia

AU - Bodó, Eniko

AU - Hagen, Evelin

AU - Bíró, Tamás

AU - Arck, Petra C.

AU - Paus, Ralf

PY - 2007/1/1

Y1 - 2007/1/1

N2 - Stress alters murine hair growth, depending on substance P-mediated neurogenic inflammation and nerve growth factor (NGF), a key modulator of hair growth termination (catagen induction). Whether this is of any relevance in human hair follicles (HFs) is completely unclear. Therefore, we have investigated the effects of substance P, the central cutaneous prototypic stress-associated neuropeptide, on normal, growing human scalp HFs in organ culture. We show that these prominently expressed substance P receptor (NK1) at the gene and protein level. Organ-cultured HFs responded to substance P by premature catagen development, down-regulation of NK1, and up-regulation of neutral endopeptidase (degrades substance P). This was accompanied by mast cell degranulation in the HF connective tissue sheath, indicating neurogenic inflammation. Substance P down-regulated immunoreactivity for the growth-promoting NGF receptor (TrkA), whereas it up-regulated NGF and its apoptosis- and catagen-promoting receptor (p75NTR). In addition, MHC class I and β2-microglobulin immunoreactivity were up-regulated and detected ectopically, Indicating collapse of the HF immune privilege. In conclusion, we present a simplistic, but instructive, organ culture assay to demonstrate sensitivity of the human HF to key skin stress mediators. The data obtained therewith allow one to sketch the first evidence-based biological explanation for how stress may trigger or aggravate telogen effluvium and alopecia areata.

AB - Stress alters murine hair growth, depending on substance P-mediated neurogenic inflammation and nerve growth factor (NGF), a key modulator of hair growth termination (catagen induction). Whether this is of any relevance in human hair follicles (HFs) is completely unclear. Therefore, we have investigated the effects of substance P, the central cutaneous prototypic stress-associated neuropeptide, on normal, growing human scalp HFs in organ culture. We show that these prominently expressed substance P receptor (NK1) at the gene and protein level. Organ-cultured HFs responded to substance P by premature catagen development, down-regulation of NK1, and up-regulation of neutral endopeptidase (degrades substance P). This was accompanied by mast cell degranulation in the HF connective tissue sheath, indicating neurogenic inflammation. Substance P down-regulated immunoreactivity for the growth-promoting NGF receptor (TrkA), whereas it up-regulated NGF and its apoptosis- and catagen-promoting receptor (p75NTR). In addition, MHC class I and β2-microglobulin immunoreactivity were up-regulated and detected ectopically, Indicating collapse of the HF immune privilege. In conclusion, we present a simplistic, but instructive, organ culture assay to demonstrate sensitivity of the human HF to key skin stress mediators. The data obtained therewith allow one to sketch the first evidence-based biological explanation for how stress may trigger or aggravate telogen effluvium and alopecia areata.

UR - http://www.scopus.com/inward/record.url?scp=38349078214&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=38349078214&partnerID=8YFLogxK

U2 - 10.2353/ajpath.2007.061206

DO - 10.2353/ajpath.2007.061206

M3 - Article

VL - 171

SP - 1872

EP - 1886

JO - American Journal of Pathology

JF - American Journal of Pathology

SN - 0002-9440

IS - 6

ER -