Mast cell mediators other than histamine induce pruritus in atopic dermatitis patients: a dermal microdialysis study

  title={Mast cell mediators other than histamine induce pruritus in atopic dermatitis patients: a dermal microdialysis study},
  author={Roman Rukwied and Grischa Lischetzki and Francis McGlone and Gisela Heyer and Martin Schmelz},
  journal={British Journal of Dermatology},
While histamine is the crucial mediator of pruritus in type 1 allergic reactions, its role in atopic dermatitis (AD) is unclear. In this study, the role of mast cell mediators in protein extravasation and pruritus was evaluated using intradermal microdialysis. The microdialysis capillaries were used to apply the mast cell degranulating substance compound 48/80 (C48/80; 0·05%) or histamine (0·01%) and also to deliver H1‐blockers (cetirizine, 200 μg mL−1) in nine AD patients and nine controls… 
Neuromediators and inflammation
  • J. Ansel
  • Biology, Medicine
    Experimental dermatology
  • 2001
It is proved that after H1 receptor blockade itch due to mast cell depletion is abolished in healthy subjects but not in patients suffering from atopic dermatitis, as well as other mediators, also released from mast cells, must be responsible for the itching in this disease.
Mast cell mediators other than histamine induced pruritus in atopic dermatitis patients – a dermal microdialysis study
  • M. Greaves
  • Medicine, Biology
    The British journal of dermatology
  • 2000
In this issue, Schmelz and colleagues from Erlangen use dermal microdialysis to demonstrate reduced extravasation of protein from the microcirculation of the skin in atopic dermatitis patients in response to intradermal delivery of histamine and the chemical histamine liberator, compound 48/80.
Mast cell chymase is increased in chronic atopic dermatitis but not in psoriasis
It is suggested that mast cell chymase may play an integral part in eliciting and maintaining cutaneous inflammation in AD but not in psoriasis, which enhances the skin’s permeability to allergens and microbes and thereby aggravates the eczema.
Neuronal sensitization for histamine-induced itch in lesional skin of patients with atopic dermatitis.
The results suggest a decreased activation of peripheral pruriceptors in patients with atopic dermatitis, and the massively increased itch in lesional skin of patients with AD might be based on sensitization for itch in the spinal cord rather than in primary afferent neurons.
Pathophysiology of pruritus in atopic dermatitis: an overview
This review highlights the recent knowledge of different mechanisms which may be involved in regulating pruritus in patients with AD potentially leading to new therapeutic applications for the treatment of itch in AD.
Neuroimmunological Mechanism of Pruritus in Atopic Dermatitis Focused on the Role of Serotonin
  • Kwangmi Kim
  • Medicine, Biology
    Biomolecules & therapeutics
  • 2012
Clinical and experimental reports suggest the possibility that antipruritic effects of selective serotonin reuptake inhibitors in atopic dermatitis patients might be at least partly due to their suppressive effect on T cells.
Stigmasterol Alleviates Cutaneous Allergic Responses in Rodents
Stigmasterol demonstrates significant potential as a molecule of interest in allergic skin disease therapy as well as suppressive effect on immunoglobulin E-mediated active cutaneous anaphylaxis, compound 48/80-induced pruritus, and irritant dermatitis induced by 12-O-tetradecanoylphorbol-13-acetate.
Histamine and antihistamines in atopic dermatitis.
The role of histamine in AD and the efficacy of antihistamines in its treatment is assessed based on results of basic research and clinical studies.


Patients' perception of itch induced by histamine, compound 48/80 and wool fibres in atopic dermatitis.
The itch and flare responses of AD patients did not correlate significantly with clinical itch intensity, eczema score or serum IgE level and their ability to discriminate between weak and strong histamine concentrations did not differ significantly.
Topical tiacrilast, a potent mast cell degranulation inhibitor, does not improve adult atopic eczema.
The data suggest that mast cells may not play a major role in the maintenance of atopic eczema lesions, and a topically applied 3% hydrogel formulation of tiacrilast against vehicle against vehicle was generally well tolerated by all patients.
Pruritogenic effects of mitogen-stimulated peripheral blood mononuclear cells in atopic eczema.
Evidence is provided that as yet unidentified mononuclear cell products may be involved in whealing and itching associated with atopic eczema.
Acetylcholine induces different cutaneous sensations in atopic and non-atopic subjects.
Evidence is provided that Ach may play an important role in the etiology of pruritus in atopic eczema patients and that the cutaneous sensations significantly differed after Ach-injection.
Role of Antigen-Induced Cytokine Release in Atopic Pruritus
Data show that leukocytes selectively release IL-8 in response to in vitro antigen stimulation, providing additional support for the concept that as yet to be identified products play a role in atopic pruritus.
Histamine and cutaneous nociception: histamine-induced responses in patients with atopic eczema, psoriasis and urticaria.
All "acute" patients showed a diminished axon-reflex function, possibly due to a downregulation of C-fiber responsiveness to histamine or an increased turnover rate of inflammatory mediators, suggesting altered central nervous processing of itch.
Histamine, antihistamines and atopic eczema
  • H. Behrendt, J. Ring
  • Medicine, Biology
    Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
  • 1990
Review of the literature shows that there are studies demonstrating a clear‐cut antipruritic effect of non‐sedating H1 antagonists, and newer studies show that cetirizine exerts an additional inhibitory effect on eosinophils, which may broaden the therapeutic spectrum of this H1 antagonist in diseases with eOSinophil involvement.
Skin reactivity to neuropeptides in atopic dermatitis
It is suggested that this hyporesponsiveness in AD is the result of natural tachyphylaxis of the target structures (mast cells and blood vessels) and possibly due to a higher availability of neuropeptides in the skin or to a primary abnormal sensitivity of the blood vessels and mast cells to these peptides.