BackgroundPovidone‐iodine (PVP‐I) is well known as an antiseptic and exhibits extensive activity against various pathogens. However, due to its uniquely unpleasant nature, it cannot be used locally to deactivate various sinonasal pathogens. Therefore, we developed a PVP‐I composite that blocks the unpleasant odor of PVP‐I for use as a local antiseptic in the sinonasal cavity and evaluated its effect on bacterial biofilm's formation and elimination in in vivo and in vitro models.MethodsMTT, lactate dehydrogenase, and live/dead staining assay were performed to examine the cellular toxicity of PVP‐I composites on the primary human nasal epithelial and RPMI 2650 cells. Crystal violet assay was performed to quantify bacterial biofilm after treating with various agents, including PVP‐I and antibiotics. Hematoxylin‐and‐eosin staining, live/dead staining assay, and scanning electron microscopy were conducted to evaluate the effect of PVP‐I on biofilm formation in a mice biofilm model.ResultsIt was observed that the PVP‐I composite did not have any significant toxic effect on the nasal epithelial cells. Furthermore, the PVP‐I composite effectively inhibited the formation of bacterial biomass within a dose‐dependent manner after 48 hours of incubation with Pseudomonas aeruginosa and Staphylococcus aureus. In mice, it effectively eliminated biofilm from the mucosa of the nasal cavity and maxillary sinus at the tested concentrations.ConclusionThe results of this study indicate that the PVP‐I composite is a promising compound that could be used locally to prevent the formation of biofilms and to eliminate them from the sinonasal cavity.

Background Exposure to airborne urban particulate matter (UPM) has been closely related to the development and aggravation of respiratory disease, including sinonasal disorders. Objective The aims of this study were to investigate the effect of UPM on nasal epithelial tight junctions (TJs) and mucosal barrier function and delineate the underlying mechanism by using both in vitro and in vivo models. Methods In this study, human nasal epithelial cells (hNECs) and BALB/c mice were exposed to UPMs. UPM 1648a and 1649 b were employed. TJ and endoplasmic reticulum (ER) stress marker expression was measured using western blot analysis and immunofluorescence. TJ integrity and nasal epithelial barrier function were evaluated by transepithelial electric resistance (TER) and paracellular flux. In addition, the effects of N‐acetyl‐L‐cysteine (NAC) on UPM-induced nasal epithelial cells were investigated. Results UPM significantly impaired the nasal epithelial barrier, as demonstrated by decreased protein expression of TJ and ER stress markers in human nasal epithelial cells. This finding was in parallel to reduced transepithelial electrical resistance and increased fluorescein isothiocyanate–dextran permeability. Pretreatment with NAC decreased the degree of UPM-mediated ER stress and restored nasal epithelial barrier disruption in human nasal epithelial cells (hNEC) and the nasal mucosa of experimental animals. Conclusion These data suggest that UPMs may induce nasal epithelial barrier dysfunction by targeting TJs and ER stress could be related in this process. Based on these results, we suggest that suppression of this process with an inhibitor targeting ER stress responses could represent a novel promising therapeutic target in UPM-induced sinonasal disease.

BackgroundMoxibustion therapy has been used historically for thousands of years and there are many clinical trials supporting its efficacy and effectiveness for various conditions. Moxa smoke has been a major reason for avoiding moxibustion due to its smell and potential risks to the human body.Methods10 units of commercial indirect moxa (CIM) from six manufacturers (A–F) were burnt in a 2.5×2.5×2.5 m chamber without ventilation, and concentrations of carbon oxides (CO and CO2), nitrogen oxides (NOx), and volatile organic compounds (VOCs) from the indoor air samples were measured.ResultsFor brands A, B, C, D, E, and F, respectively, relative to baseline values, we observed an increase in CO (from 0.002 to 0.007, 0.006, 0.005, 0.006, 0.005, and 0.006 parts per billion (ppb)), NOx (from 0.009 to 0.051, 0.025, 0.015, 0.050, 0.019, and 0.020 ppb), and total VOCs (TVOC; from 48.06 to 288.83, 227.93, 140.82, 223.22, 260.15, and 161.35 μg/m3), while the concentration of CO2 was not elevated. Each CIM brand demonstrated different VOC emission characteristics, which could be divided into three groups. On average, we estimated that 20 units of CIM or 2.41 g moxa floss would need to be combusted in order to exceed the safe levels set by Korean environmental law. This limit is likely to be greater in the case of a larger room or use of ventilation.ConclusionsDespite increased CO/NOx/VOC concentrations, overall levels remained within safe limits. These findings may help clinicians to maintain safe moxibustion treatment conditions to help keep both patients and clinicians safe from the pollutants generated by moxa combustion.

Purpose: Chronic rhinosinusitis with nasal polyps (CRSwNP) is a complex inflammatory disease of the nasal and paranasal sinus mucosa. The disease is associated with mitochondrial dysfunction, structural changes in the mitochondria, and reactive oxygen species (ROS) generation. This study investigated whether there are functional and morphological changes in the mitochondria in the epithelial cells of nasal polyps (NPs) and Staphylococcus aureus enterotoxin B (SEB)-stimulated nasal epithelial cells. Methods: In all, 30 patients with CRSwNP and 15 healthy subjects were enrolled. Mitochondrial ROS (mtROS) and changes in mitochondrial functions and structures were investigated in the uncinate tissue (UT) of healthy controls, the UT or NPs of CRSwNP patients, and human nasal epithelial cells with or without SEB stimulation. Results: Oxidative phosphorylation complexes showed various responses following SEB stimulation in the nasal epithelial cells, and their expressions were significantly higher in the NPs of patients with CRSwNP than in the UT of controls. Generation of mtROS was increased following SEB exposure in nasal epithelial cells and was reduced by pretreatment with MitoTEMPO, which is used as an mtROS scavenger. In the tissues, mtROS was significantly increased in the NPs of CRSwNP patients compared to the UT of controls or CRSwNP patients. The expressions of fusion-and fission-related molecules were also significantly higher in SEB-exposed nasal epithelial cells than in non-exposed cells. In tissues, the expression of fission (fission mediator protein 1)-and fusion (membrane and mitofusin-1, and optic atrophy protein 1)-related molecules was significantly higher in the NPs of CRSwNP patients than in UT of controls or CRSwNP patients. Transmission electron microscopy revealed elongated mitochondria in SEB-exposed nasal epithelial cells and epithelial cells of NPs.

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.