The macrophage mannose receptor (MMR) and toll-like receptor 2 (TLR2) and 4 (TLR 4) in chronic sinus disease - 25/08/11
Abstract |
Rationale |
Innate pattern recognizing receptors (MMR, TLR 2 and TLR4), capable of recognizing pathogen recognizing molecular patterns and signal transduction for proinflammatory mechanisms, might have an important role in immune interactions in chronic sinus disease.
Methods |
Surgical samples from patients with chronic rhinosinusitis (CS, n=10), nasal polyps (NPs, n=10) and controls (turbinate tissue, n=10) were investigated with real time RT-PCR for MMR, TLR 2 and TLR4 mRNA expression and the presence and location of MMR positive cells was analyzed by immunohistochemistry.
Results |
Quantification of MMR mRNA showed a statistically significant higher expression in NPs compared to CS (p=0.04) and controls (p=0.001). Although immunohistochemistry revealed expression of MMR in all tissue samples, only in NP we found an enhanced positive cellular staining including cell aggregates. Quantification of TLR 2 and TLR 4 mRNA showed no difference of expression in CS compared to NP. Yet, TLR-2 and TLR-4 mRNA expression in nasal tissues were significantly correlated (r=0.57, p=0.001) and was found in all tissue samples.
Conclusions |
We demonstrated for the first time that the expression of MMR is significantly up-regulated in NP compared to patients with CS or turbinate tissue of controls. Macrophages expressing MMR, accumulated in cell aggregates in NP, play a possible key role in pathogen-macrophage interaction in NP disease. Toll-like receptor expression in all sino-nasal tissue illustrates their possibly important immunological sentinel function in upper airway mucosa.
El texto completo de este artículo está disponible en PDF. Funding: Alphonse and Jean Forton for Cystic Fibrosis |
Vol 113 - N° 2S
P. S49 - février 2004 Regresar al númeroBienvenido a EM-consulte, la referencia de los profesionales de la salud.
El acceso al texto completo de este artículo requiere una suscripción.
¿Ya suscrito a @@106933@@ revista ?