Abstract
Povidone-iodine (PVP-I) is an antiseptic and a disinfectant with broad-spectrum antimicrobial activity against various pathogens. However, it is unclear whether PVP-I nasal instillation can suppress mucosal inflammation in non-eosinophilic chronic rhinosinusitis (CRS) mice. This study aimed to explore the anti-inflammatory effects and underlying molecular mechanism of PVP-I on lipopolysaccharide-stimulated airway epithelial cells and investigate whether nasal instillation of PVP-I can suppress mucosal inflammation in non-eosinophilic CRS mice. Inflammation-related molecules in the nasal epithelial cells and non-eosinophilic CRS mice were measured by enzyme-linked immunosorbent assay, western blotting, quantitative real-time polymerase chain reaction, immunoprecipitation, and histopathological analysis. PVP-I blocked expressions of various inflammation-related molecules, such as NLRP3, NF-κB-p65, caspase-1, and IL-1β. Translocation of NF-κB to the nucleus, and assembly of NLRP3/ASC complexes in the nasal epithelial cells and non-eosinophilic CRS mice were also restricted. Notably, PVP-I strongly blocked the receptor co-localization of TLR4 and MyD88 in the epithelial cells of nasal mucosa. We demonstrated that PVP-I significantly attenuated inflammatory molecules and cytokines via blocking the formation of TLR4 and MyD88 complexes during LPS-induced mucosal inflammation in non-eosinophilic CRS.
Highlights
Chronic rhinosinusitis (CRS) is a persistent inflammatory disease of the nasal and paranasal sinuses mucosa[1]
Protein expression of NLRP3 were elevated in the LPS and ATP (LPS/ATP) treated cells compared with cells treated with LPS or ATP alone (Supplementary Fig. S1b)
Expressions of NLRP3 mRNA were significantly elevated in LPS/ATP treated cells compared with cells treated with each alone (Supplementary Fig. S1c)
Summary
Chronic rhinosinusitis (CRS) is a persistent inflammatory disease of the nasal and paranasal sinuses mucosa[1]. The selective expression of type 1, 2, or 3 immune responses is associated with increasing CRS heterogeneity[5–8]. An endotype of CRS with prominent type 2 immune responses is associated with eosinophilic infiltration into sinonasal mucosa and can benefit from treatment with systemic steroids and biologics, whereas non-eosinophilic CRS shows resistance to these t herapy[9–12]. NLRP3 inflammasomes play essential roles in the innate and adaptive immune responses serving as a pattern-recognition receptor and a trigger for caspase-1 activation and the maturation of IL-1β and IL-1814,15. The NLRP3 and its downstream IL-1β were identified as potent inducers of neutrophilic inflammation in various inflammatory d iseases[16,17]. Previous studies showed that NLRP3 was highly expressed in nasal polyps (NPs) from subjects with CRSwNP, and significantly correlated with neutrophilic nasal p olyps[18,19]. PVP-I was more effective in non-eosinophilic CRS than its eosinophilic
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