Proteinase-Activated Receptor-2 Mediates Itch: A Novel Pathway for Pruritus in Human Skin

We examined whether neuronal proteinase-activated receptor-2 may be involved in pruritus of human skin

Martin Steinhoff


Scholarcy highlights

  • Recent findings on a specific pathway for itch have clarified the neurophysiological basis for pruritus
  • Codeine-induced mediator release In atopic dermatitis patients, codeine-induced tryptase release exceeded by far the control values, as can be judged in the dose–response relationship
  • Stimulated tryptase release in AD patients was more pronounced at codeine concentrations of Ն0.3 mg and reached approximately fourfold higher values after maximum stimulation with codeine
  • After the identification of proteinase-activated receptor-2 on afferent nerve fibers, the role of proteinase-activated receptors in the pain pathway has become of major interest
  • The recent finding that, in AD patients, itch upon degranulation of mast cells could not be suppressed by antihistamines suggested that mast cell mediators other than histamine could act as important itch mediators in AD
  • In line with these observations, our results indicate increased signaling via PAR-2 in AD patients, which is characterized by the release of a higher concentration of the putative endogenous PAR-2 agonist mast cell tryptase, a higher density of PAR-2 on epidermal nerves, keratinocytes, and endothelia, and enhanced responsiveness of the patients toward exogenously applied PAR-2 agonist
  • Even the nonactive reverse peptide provoked itch in patients and controls, probably because of mast cell activation

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