Loss of dipeptidylpeptidase IV activity in chronic rhinosinusitis contributes to the neurogenic inflammation induced by substance P in the nasal mucosa

Détails

ID Serval
serval:BIB_40F9F61C4CD5
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Loss of dipeptidylpeptidase IV activity in chronic rhinosinusitis contributes to the neurogenic inflammation induced by substance P in the nasal mucosa
Périodique
FASEB Journal
Auteur(s)
Grouzmann  E., Monod  M., Landis  B., Wilk  S., Brakch  N., Nicoucar  K., Giger  R., Malis  D., Szalay-Quinodoz  I., Cavadas  C., Morel  D. R., Lacroix  J. S.
ISSN
1530-6860 (Electronic)
Statut éditorial
Publié
Date de publication
07/2002
Volume
16
Numéro
9
Pages
1132-4
Notes
Journal Article --- Old month value: Jul
Résumé
In this study, we have found that dipeptidylpeptidase IV (DPPIV) plays in vivo an active role in the modulation of the inflammatory response of chronic rhinosinusitis. Human nasal mucosa expresses DPPIV-like immunoreactivity in submucosal seromucus glands, leukocytes, and endothelial cells of blood vessels. DPPIV enzymatic activity in nasal tissue biopsies taken from patients suffering from chronic rhinosinusitis was correlated inversely with the density of inflammatory cells in the nasal mucosa, and the DPPIV activity rose when chronic rhinosinusitis was treated. By using a pig animal model, we have shown that the intranasal administration of recombinant DPPIV decreased the vasodilatation induced by exogenous substance P (SP), a proinflammatory peptide released by sensory nerves. In contrast, an inhibitor of DPPIV enhanced the vasodilatatory effect at low doses of SP. SP5-11 was 100- to 1000-fold less potent than SP as a vasodilator of the nasal mucosa. The vasodilatatory effect of SP was abolished by a NK1 receptor antagonist. In conclusion, these results suggest a new pathophysiological pathway for rhinitis based on clinical observations in humans, indicating the involvement of an enzyme to modulate non-adrenergic and non-cholinergic substrate that occurred during nasal dysfunctions.
Mots-clé
Animals Antigens, CD26/*metabolism Chronic Disease Humans Models, Biological Nasal Mucosa/blood supply/drug effects/*enzymology Rhinitis/chemically induced/*enzymology/pathology Substance P/pharmacology Swine Vascular Resistance/drug effects Vasodilator Agents/pharmacology
Pubmed
Web of science
Création de la notice
28/01/2008 11:35
Dernière modification de la notice
03/03/2018 16:30
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