Increased expression of dectin-1 in nasal polyps

• Published in: American journal of otolaryngology Vol. 34; no. 3; pp. 183 - 187
• Main Authors: Gong, Jian, MD, Wang, Pei, MD, Qiu, Ze-heng, MD, Chen, Qiu-jian, MD
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.05.2013; Elsevier Limited
• Subjects: Adult; Blotting, Western; Bone; Cytokines; Enzyme-Linked Immunosorbent Assay; Female; Humans; Immune system; Interleukin-4 - metabolism; Interleukin-5 - metabolism; Lectins, C-Type - metabolism; Life sciences; Male; Nasal Polyps - metabolism; Otolaryngology; Pathogenesis; Pattern recognition; Proteins; Real-Time Polymerase Chain Reaction; Software; Statistical analysis; Studies; Surgery; Turbinates - metabolism
• ISSN: 0196-0709; 1532-818X
• DOI: 10.1016/j.amjoto.2012.10.003

Abstract Purpose A fungal etiology has been proposed to underlie severe nasal polyps (NP). Dectin-1 is an innate immune pattern recognition receptor which is involved in the recognition of some pathogenic fungi. We investigated the Dectin-1 levels in NP in order to evaluate the implication of such expression with respect to the development of NP. Materials and methods Normal inferior turbinate tissues were obtained from forty patients undergoing surgery for augmentation rhinoplasty. Nasal polyp tissues were obtained from 53 patients who underwent endoscopic sinus surgery for chronic polypoid rhinosinusitis. Real-time polymerase chain reaction and Western blot analysis were performed to evaluate the mRNA and protein level of Dectin-1, respectively. ELISA was carried out to evaluate the cytokine production (IL-4, IL-5, IL-10, and TNF-α) in NP. Results Real-time polymerase chain reaction and Western-blot analysis showed that Dectin-1 expression in NP was increased compared with that in normal nasal inferior turbinate tissues. ELISA results suggest that the local expression of type-1 and type-2 inflammatory cytokine is skewed toward type-2 inflammatory cytokine in NP. Conclusions These results suggest that Dectin-1 may play a role in the development of NP, and the production of Dectin-1, IL-4 and IL-5 (type-2 cytokines), may mainly participate in the inflammatory reaction in NP.