Pruritus is one of cardinal symptoms of atopic dermatitis, the control of itching
is important in its treatment. Its molecular mechanisms remain largely unexplained.
Certainly, an itch–scratch vicious cycle, in which scratch irritation enhances itch,
is at work in atopic patients [
[1]
]. A defective epidermal barrier due to a marked decrease of ceramide in atopic dermatitis
allows the penetration of allegens through the skin, facilitating the interaction
of these allergens with the local antigen-presenting cells and immune-effector cells
[
[2]
]. Disturbed skin-barrier function in atopic dermatitis is at least partly related
to a disturbed lipid composition of the stratum corneum. A significant reduction in
ceramides has been found in lesional as well as non-lesional skin of atopic dermatitis
patients [
[3]
]. A novel enzyme moreover, glucosylceramide/sphingomyelin (GCer-SM) deacylase, which
cleaves the N-acyl linkage sphingomyelin and glucosylceramide, has been found in atopic
dermatitis patients. Due to this enzyme's activity, the level of sphingosylphosphorylcholine
in the stratum corneum of atopic dermatitis patients is high in comparison with that
in normal skin [
[2]
]. Recently, we reported that SPC, a breakdown product of sphingomyelin, induced the
itch–scratch response in mice [
[4]
].Keywords
To read this article in full you will need to make a payment
Purchase one-time access:
Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online accessOne-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:
Subscribe to Journal of Dermatological ScienceAlready a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
References
- Itch.Lancet. 2003; 361: 690-694
- A possible mechanism underlying the ceramide deficiency in atopic dermatitis: expression of a deacylase enzyme that cleaves the N-acyl linkage of sphingomyelin and glucosylceramide.J Dermatol Sci. 2009; 55: 1-9
- Decreased level of ceramides in stratum corneum of atopic dermatitis: an etiologic factor in atopic dry skin?.J Invest Dermatol. 1991; 96: 523-526
- Characterizations of sphingosylphosphorylcholine-induced scratching responses in ICR mice using naltrexon, capsaicin, ketotifen and Y-27632.Eur J Pharmacol. 2008; 583: 92-96
- Leukotriene B(4) mediates sphingosylphosphorylcholine-induced itch-associated responses in mouse skin.J Invest Dermato. 2009;
- Lysophosphatidic acid (LPA) induces plasma exudation and histamine release in mice via LPA receptors.J Pharmacol Sci. 2006; 100: 82-87
- Lysophosphatidic acid induces histamine release from mast cells and skin fragments.Pharmacology. 2005; 75: 13-20
- Involvement of unique mechanisms in the induction of scratching behavior in BALB/c mice by compound 48/80.Eur J Pharmacol. 2002; 448: 175-183
- The multi-functional role of sphingosylphosphorylcholine.Prog Lipid Res. 2008; 47: 62-75
- Involvement of the BLT2 receptor in the itch-associated scratching induced by 12-(S)-lipoxygenase products in ICR mice.Br J Pharmacol. 2008; 154: 1073-1078
Article info
Publication history
Published online: July 12, 2010
Received:
May 4,
2009
Identification
Copyright
© 2009 Japanese Society for Investigative Dermatology. Published by Elsevier Inc. All rights reserved.
