The transmembrane protein Dectin-1 appears to play a role in the pathogenesis of nasal polyposis (NP), providing a potential new target for treating the condition, report Chinese researchers.
Both protein and mRNA levels of Dectin-1 were substantially elevated in NP tissue, compared with in normal nasal tissue in an analysis conducted by Qiu-jian Chen (Sun Yat-Sen University, Guangzhou, China) and team.
"To the authors' knowledge, this is the first study to show the presence of Dectin-1 in NP," they write in the American Journal of Otolaryngology.
Chen et al explain that Dectin-1 is an innate immune pattern recognition receptor involved in the detection of some pathogenic fungi. And, although some studies have suggested that immunopathogenic mechanisms underlie the immune response in NP, little is known about the expression of Dectin-1 in NP.
For the current study, the team obtained samples from the normal inferior turbinate tissue of 40 patients who were having surgery for augmentation rhinoplasty and compared these with NP samples obtained from 53 patients undergoing surgery for chronic polyploid rhinosinusitis.
Chen and team found that the mRNA expression level of Dectin-1 was significantly upregulated in NP tissue compared with in the normal nasal tissue, as indicated by real-time polymerase chain reaction analysis.
"This increased expression level of Dectin-1 would support our hypothesis that Dectin-1 (an innate immune component) may be involved in the pathogenic fungi in NP," say Chen and colleagues.
Furthermore, Western blot analysis reveled that the Dectin-1 protein was rarely detected in normal nasal tissue, whereas it was strongly detected in NP tissue.
As previous studies have shown that another function of Dectin-1 is the production of inflammatory cytokines, which demonstrate a cell-specific nature, the researchers used enzyme-linked immunosorbent assay (ELISA) to determine the levels of inflammatory cytokines in the two sample groups.
The team reports that expression levels of type-2 inflammatory cytokines interleukin (IL)-4 and IL-5 were significantly elevated in the NP samples compared with in the normal samples, while the type 1 cytokine IL-12 could not be detected in either sample group.
"The production of Dectin-1, IL-4 and IL-5 (type-2 cytokines), may mainly participate in the inflammatory response in NP," says the team. "Novel therapeutic agents which can prevent Dectin-1 may therefore be used in preventing the development of NP in future."
However, additional studies to find out the precise action of Dectin-1 in NP are needed, they add.
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