Role(s) of formyl-peptide receptors expressed in nasal epithelial cells

Chronic rhinosinusitis is one of the most frequent chronic diseases in humans. Little is known about stimuli initiating tissue remodeling process that determines the morphological expression of the disease. N-formyl peptide receptors (FPRs) are innate immunity receptors important in tissue remodelin...

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Published inJournal of biological regulators and homeostatic agents Vol. 25; no. 4; p. 553
Main Authors Prevete, N, Salzano, F A, Rossi, F W, Rivellese, F, Dellepiane, M, Guastini, L, Mora, R, Marone, G, Salami, A, De Paulis, A
Format Journal Article
LanguageEnglish
Published Italy 01.10.2011
Subjects
Cell Line, Tumor
Cell Movement
Chemotaxis - drug effects
Humans
N-Formylmethionine Leucyl-Phenylalanine - pharmacology
Nasal Mucosa - physiology
Oligopeptides - pharmacology
Receptors, Formyl Peptide - genetics
Receptors, Formyl Peptide - physiology
Receptors, Lipoxin - genetics
Receptors, Urokinase Plasminogen Activator - physiology
RNA, Messenger - analysis
Transforming Growth Factor beta - genetics
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Summary:Chronic rhinosinusitis is one of the most frequent chronic diseases in humans. Little is known about stimuli initiating tissue remodeling process that determines the morphological expression of the disease. N-formyl peptide receptors (FPRs) are innate immunity receptors important in tissue remodeling of gastric and intestinal epithelium. The expression and functions of FPRs in nasal epithelial cells were examined to evaluate whether they could be important in the remodeling of nasal mucosa. The aim of this study is to examine FPR expression in a nasal epithelial cell line (RPMI-2650) at mRNA and protein levels. To determine whether FPRs were functional, chemotaxis experiments were carried out. In addition the effects of FPRs agonists on the expression (PCR and ELISA) of VEGF-A and TGF-beta, two key mediators of tissue remodelling, were examined. Here we demonstrate that RPMI-2650 express FPR and FPRL2, but not FPRL1. fMLP, a bacterial product active on FPR, and uPAR(84-95), an inflammatory mediator agonist for FPRL2, stimulated migration of nasal epithelial cells. fMLP and uPAR(84-95) induce expression and secretion of VEGF-A and TGF-beta. Our results suggest a possible mechanisms initiating tissue remodeling observed during chronic rhinosinusitis. This study provides further evidence that FPRs play a more complex role in human pathophysiology than bacterial recognition.
ISSN:0393-974X