Background and Objectives: Fine particulate matter, PM_2.5, is becoming a major threat to human health, particularly in terms of respiratory diseases. Pyroptosis is a recently discovered and distinct form of cell death, characterized by pore formation in the cell membrane and secretions of proinflammatory cytokines. There has been little research on the effect of PM_2.5 on pyroptosis, especially in airway epithelium. We investigated whether PM_2.5-related oxidative stress induces pyroptosis in bronchial epithelial cells and defined the underlying mechanisms. Materials and Methods: After exposure of a BEAS-2B cell line to PM_2.5 concentration of 20 µg/mL, reactive oxygen species (ROS) levels, parameters related to pyroptosis, and NF-κB signaling were measured by Western blotting, immunofluorescence, and ELISA (Enzyme-linked immunosorbent assay). Results: PM_2.5 induced pyroptotic cell death, accompanied by LDH (Lactate dehydrogenase) release and increased uptake of propidium iodide in a dose-dependent manner. PM_2.5 activated the NLRP3-casp1-gasdermin D pathway, with resulting secretions of the proinflammatory cytokines IL-1β and IL-18. The pyroptosis activated by PM_2.5 was alleviated significantly by NLRP3 inhibitor. In PM_2.5-exposed BEAS-2B cells, levels of intracellular ROS and NF-κB p65 increased. ROS scavenger inhibited the expression of the NLRP3 inflammasome, and the NF-κB inhibitor attenuated pyroptotic cell death triggered by PM_2.5 exposure, indicating that the ROS/NF-κB pathway is involved in PM_2.5-induced pyroptosis. Conclusions: These findings show that PM_2.5 exposure can cause cell injury by NLRP3-inflammasome-mediated pyroptosis by upregulating the ROS/NF-κB pathway in airway epithelium.

Background and Objectives: Air pollution, particularly particulate matter (PM), has a variety of adverse effects on human health. PM is known to induce cell death through various pathways, including pyroptosis. Despite its significance, research on PM-induced pyroptosis in nasal epithelial cells remains limited. This study aimed to explore PM-induced pyroptosis in cultured human nasal epithelial cells.Methods: For the in vitro experiments, human nasal epithelial cells were cultured. Cell viability was assessed using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, while cell death was evaluated through propidium iodide (PI) staining and lactate dehydrogenase (LDH) release measurement. Protein expression levels related to pyroptosis were examined via western blot using antibodies against NOD-like receptor family, pyrin domain containing 3 (NLRP3), cleaved caspase-1 (CASP1 P20), gasdermin D (GSDMD)-N, and glyceraldehyde phosphate dehydrogenase. Immunofluorescent staining with a CASP1 P20 antibody was conducted to visualize cellular localization. Enzyme-linked immunosorbent assay was utilized to quantify interleukin (IL)-1β and IL-18 protein levels.Results: Treatment with PM resulted in decreased cell viability, elevated LDH release, and intensified PI staining, indicating cell death. Pyroptosis was confirmed by the elevated expression of NLRP3, CASP1 P20, and GSDMD-N, along with increased levels of IL-1β and IL-18. Inhibiting the NLRP3 inflammasome with MCC950 reduced the PM-induced effects on protein expression and cytokine release, highlighting the role of the NLRP3 inflammasome in PM-triggered pyroptosis in human nasal epithelial cells.Conclusion: We showed that PM triggers pyroptosis in human nasal epithelial cells, driven by NLRP3 inflammasome-dependent signaling pathways.

Pyroptosis represents a type of cell death mechanism notable for its cell membrane disruption and the subsequent release of proinflammatory cytokines. The Nod-like receptor family pyrin domain containing inflammasome 3 (NLRP3) plays a critical role in the pyroptosis mechanism associated with various diseases resulting from particulate matter (PM) exposure. Tert-butylhydroquinone (tBHQ) is a synthetic antioxidant commonly used in a variety of foods and products. The aim of this study is to examine the potential of tBHQ as a therapeutic agent for managing sinonasal diseases induced by PM exposure. The occurrence of NLRP3 inflammasome-dependent pyroptosis in RPMI 2650 cells treated with PM < 4 µm in size was confirmed using Western blot analysis and enzyme-linked immunosorbent assay results for the pyroptosis metabolites IL-1β and IL-18. In addition, the inhibitory effect of tBHQ on PM-induced pyroptosis was confirmed using Western blot and immunofluorescence techniques. The inhibition of tBHQ-mediated pyroptosis was abolished upon nuclear factor erythroid 2-related factor 2 (Nrf2) knockdown, indicating its involvement in the antioxidant mechanism. tBHQ showed potential as a therapeutic agent for sinonasal diseases induced by PM because NLRP3 inflammasome activation was effectively suppressed via the Nrf2 pathway.

Polycaprolactone (PCL) has emerged as a promising biomaterial for artificial heart applications due to its biodegradability and mechanical properties. However, its hydrophobic nature and limited biocompatibility pose challenges for cardiovascular applications, requiring optimal cell-material interactions. This study investigates the surface modification of silk fibroin-derived peptide/PCL coatings to enhance biocompatibility and cellular response for potential artificial heart applications. PCL substrates were blended with varying concentrations of silk fibroin-derived peptide (0.2%, 0.5%, and 1% w/v). Surface characterization was performed using water contact angle measurements, Fourier transform infrared spectroscopy (FTIR), and scanning electron microscopy. Biocompatibility was evaluated through cell viability assays and CD31 expression analysis. Silk fibroin-derived peptide incorporation significantly improved surface hydrophilicity, with contact angles decreasing from 78° (bare PCL) to 62° (1% silk fibroin-derived peptide). FTIR analysis confirmed successful incorporation of silk fibroin-derived peptides, showing characteristic PCL ester C=O absorption at ∼1720 cm−1 and concentration-dependent amide I contributions at ∼1630–1670 cm−1. Cell viability studies demonstrated enhanced cellular response with increasing silk fibroin-derived peptide concentration, particularly evident at day 7. CD31 expression analysis revealed improved endothelial marker expression, with the highest levels observed on 1% silk fibroin-derived peptide-incorporated substrates. The results demonstrate that silk fibroin blended to PCL significantly enhances biocompatibility through improved hydrophilicity and cellular interactions. Taken together, these preliminary results indicate that silk fibroin-derived peptide-incorporated PCL could represent a promising biomaterial platform for artificial heart applications, with the potential to improve endothelial compatibility and support endothelialization.

Background and Objectives: Eosinophilic chronic rhinosinusitis with nasal polyps (ECRSwNP) is characterized by type 2 inflammation, prominent eosinophil accumulation, and enhanced epithelial–mesenchymal transition (EMT). Although interleukin (IL)-5 plays a central role in eosinophil differentiation and activation, its involvement in driving EMT in human nasal epithelial cells (HNECs) remains unclear. This study investigated IL-5 receptor α (IL-5Rα)–mediated signaling and EMT profiles in ECRSwNP, aiming to determine whether IL-5–activated eosinophil-like cells promote EMT in HNECs.Methods: Nasal tissues from healthy controls, non-ECRSwNP patients, and ECRSwNP patients (n=12 per group) were analyzed using hematoxylin and eosin staining, quantitative real-time polymerase chain reaction, immunohistochemistry, and Western blotting. HL-60 promyelocytic leukemia cells were differentiated into eosinophil-like cells and subsequently stimulated with IL-5. HNECs were cocultured with undifferentiated HL-60 cells, differentiated HL-60 cells, or IL-5–stimulated differentiated HL-60 cells using a Transwell system. Expression of EMT-related markers was assessed by Western blotting and immunofluorescence.Results: ECRSwNP tissues demonstrated markedly increased eosinophil infiltration, elevated IL-4 and IL-5 transcript levels, and significantly higher expression of IL-5Rα, phosphorylated Janus kinase 2 (JAK2), and phosphorylated signal transducer and activator of transcription 5 (STAT5) compared with controls and non-ECRSwNP tissues. EMT-associated changes, characterized by reduced E-cadherin and increased vimentin expression, were most pronounced in ECRSwNP. In vitro, IL-5 stimulation enhanced IL-5Rα expression, activated JAK2/STAT5 signaling, and increased secretion of eosinophil-associated mediators in differentiated HL-60 cells. Co-culture with IL-5-stimulated eosinophil-like cells induced EMT in HNECs, whereas unstimulated HL-60 cells exerted minimal effects.Conclusion: IL-5Rα-mediated signaling is upregulated in ECRSwNP and may contribute to EMT through eosinophil-dependent mechanisms. IL-5–activated eosinophils promote EMT-related changes in HNECs, providing a mechanistic link between type 2 inflammation and epithelial remodeling. These findings suggest that IL-5Rα signaling may represent a potential therapeutic target for modulating tissue remodeling in ECRSwNP.