Nasal polyps in patients with and without cystic fibrosis: a differentiation by innate markers and inflammatory mediators.
BACKGROUND
The dysfunction of the mucosal interface of the upper respiratory tract in cystic fibrosis (CF) patients is clinically visible by the development of nasal polyps (NP) at a young age. Innate defence markers and inflammatory mediators in NP from patients with CF were compared with non-cystic fibrosis nasal polyps (non-CF-NP) to determine a possible different immunological background in macroscopically similar tissue.


METHODS
Surgical samples were obtained from patients with non-CF-NP, cystic fibrosis patients with nasal polyps (CF-NP) and control patients (CO). With real time PCR, the mRNA expression of human beta defensins (HBD) 2 and 3, toll-like receptors (TLR) 2 and 4 and the macrophage mannose receptor (MMR) were measured. On homogenates of the surgical samples eotaxin, myeloperoxidase (MPO), IL-5 and IL-8 protein content was measured using commercial ELISA kits; IgE and eosinophilic cationic protein (ECP) were measured by the Unicap system.


RESULTS
In CF-NP we found a statistically significant higher mRNA expression of HBD 2 compared with non-CF-NP and CO and of TLR 2 compared with non-CF-NP. In the non-CF-NP group, MMR mRNA expression was significantly elevated compared with CO and CF-NP. For TLR 4 mRNA expression no statistically significant differences were found between groups. IL-5 was below detection level in all CO and CF-NP, but was measurable in 80% of the non-CF-NP. MPO and IL-8 concentrations were significantly higher in CF-NP compared with CO and non-CF-NP, whereas ECP, eotaxin and IgE were significantly higher in the non-CF-NP group.


CONCLUSIONS
We here demonstrate that CF-NP and non-CF-NP not only differ in terms of inflammatory mediator profile, but also in terms of innate markers.
Claeys
S
S
Upper airways Research Laboratory, Department of Otorhinolaryngology, Ghent University, Belgium. sem.claeys@Ugent.be
Van Hoecke
H
H
Holtappels
G
G
Gevaert
P
P
De Belder
T
T
Verhasselt
B
B
Van Cauwenberge
P
P
Bachert
C
C
D000890:Anti-Infective Agents / Q000032:analysis; D015415:Biomarkers / Q000032:analysis; D003550:Cystic Fibrosis / Q000150:complications / Q000276:immunology*; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis; D015848:Interleukin-5 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D037181:Lectins, C-Type / Q000032:analysis; D008264:Macrophages / Q000276:immunology; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins / Q000032:analysis; D008562:Membrane Glycoproteins / Q000032:analysis; D009298:Nasal Polyps / Q000150:complications / Q000276:immunology*; D009195:Peroxidase / Q000032:analysis; D012333:RNA, Messenger / Q000032:analysis; D011956:Receptors, Cell Surface / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors; D023083:beta-Defensins / Q000032:analysis
D000890:Anti-Infective Agents; D015415:Biomarkers; C422950:DEFB103A protein, human; C106641:DEFB4A protein, human; D018836:Inflammation Mediators; D015848:Interleukin-5; D016209:Interleukin-8; D037181:Lectins, C-Type; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins; D008562:Membrane Glycoproteins; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; C495342:TLR2 protein, human; C495345:TLR4 protein, human; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors; D023083:beta-Defensins; D009195:Peroxidase