Abstract:
BACKGROUND:Nasal polyposis is characterized by persistent inflammation and remodeling in sinonasal mucosa. Toll-like receptor 9 (TLR9) is a DNA receptor of the innate immune system that plays a pivotal role in fibrosis and inflammatory responses. The aim of this study is to explore the expression, activity, and potential pathogenic role of TLR9 signaling in tissue remodeling in nasal polyp-derived fibroblasts (NPDFs). METHODS:Fibrotic and inflammatory responses elicited by type A CpG oligonucleotides were examined in the NPDFs by a combination of real-time quantitative polymerase chain reaction, Western blot analysis, enzyme-linked immunosorbent assay, and immunofluorescence staining. For these experiments, the NPDFs were stimulated with different TLR9 agonists (CpG A and B) and blocked with inhibitors (MyD88 inhibitor and chloroquine). RESULTS:TLR9 expression was significantly higher in nasal polyposis (NP) tissues compared to control or chronic rhinosinusitis (CRS) mucosa. In the NPDFs, TLR9 showed intracellular localization and expression of TLR9 was increased after treatment with CpG A. CpG A increased production of α-smooth muscle actin (α-SMA), fibronectin, and matrix metalloproteinases (MMPs) (MMP1, MMP2, and MMP9) in the NPDFs, while MyD88 inhibitor and chloroquine, which are known to block the TLR9 signaling pathway, inhibited their production. CpG A also produced type I interferons (IFN-α and IFN-β), which were inhibited by MyD88 inhibitor. CONCLUSION:Our data indicates that CpG A-induced fibroblast activation and cytokine production were mediated via TLR9 stimulation in NPDFs. Disrupting this process with an inhibitor targeting TLR9 or its downstream signaling pathways could represent a novel approach to CRS with NP (CRSwNP) therapy.
journal_name
Int Forum Allergy Rhinoljournal_title
International forum of allergy & rhinologyauthors
Park SK,Jin SY,Yeon SH,Lee SB,Xu J,Yoon YH,Rha KS,Kim YMdoi
10.1002/alr.22155subject
Has Abstractpub_date
2018-09-01 00:00:00pages
1001-1012issue
9eissn
2042-6976issn
2042-6984journal_volume
8pub_type
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