Conclusions. Proteases in fungi interact with nasal epithelial cells and enhance the production of inflammatory cytokines in vitro. These cytokines induced the migration of eosinophils and neutrophils. Protease-activated receptors (PARs) might also play a role in the process of epithelial cell activation. Objective. The nasal epithelium is the first barrier encountered by airborne allergens and an active participant in airway inflammation. Fungi have been increasingly recognized as important pathogens in sinusitis and consist of several allergenic proteins. Materials and methods. Nasal polyp epithelial cells were obtained from patients and stimulated with Alternaria, Aspergillus, and Cladosporium. Interleukin-8 (IL-8), granulocyte-macrophage colony stimulating factor (GM-CSF), and regulated on activation normal T expressed and secreted (RANTES) were measured to determine the activation of epithelial cells. Reverse transcriptase-polymerase chain reaction test (RT-PCR) for PAR mRNA expression in nasal epithelial cells was performed. Eosinophil and neutrophil migration was induced with nasal polyp epithelial cells conditioned media (HPECM). Results. Fungi enhanced the production of chemical mediators from nasal epithelial cells. When nasal epithelial cells were activated with fungi, PAR2 and PAR3 mRNAs were more strongly expressed than in nonactivated cells. Eosinophil migration was induced by RANTES and eotaxin, and neutrophil migration was induced by IL-8 in HPECM.

Chronic rhinosinusitis (CRS) is a diverse chronic inflammatory disease of the sinonasal mucosa. CRS manifests itself in a variety of clinical and immunologic patterns. The histological hallmark of eosinophilic CRS (ECRS) is eosinophil infiltration. ECRS is associated with severe disease severity, increased comorbidity, and a higher recurrence rate, as well as thick mucus production. Eosinophils play an important role in these ECRS clinical characteristics. Eosinophils are multipotential effector cells that contribute to host defense against nonphagocytable pathogens, as well as allergic and nonallergic inflammatory diseases. Eosinophils interact with Staphylococcus aureus, Staphylococcal enterotoxin B, and fungi, all of which were found in the tissue of CRS patients. These interactions activate Th2 immune responses in the sinonasal mucosa and exacerbate local inflammation. Activated eosinophils were discovered not only in the tissue but also in the sinonasal cavity secretion. Eosinophil extracellular traps (EETs) are extracellular microbes trapping and killing structures found in the secretions of CRS patients with intact granule protein and filamentous chromatic structures. At the same time, EET has a negative effect by causing an epithelial barrier defect. Eosinophils also influence the local tissue microenvironment by exchanging signals with other immune cells and structural cells. As a result, eosinophils are multifaceted leukocytes that contribute to various physiologic and pathologic processes of the upper respiratory mucosal immune system. The goal of this review is to summarize recent research on the immunopathologic properties and immunologic role of eosinophils in CRS.

Background: The nasal epithelium is the first barrier encountered by airborne allergens and is an active participant in airway inflammation. Fungi have been increasingly recognized as important pathogens in sinusitis and airway diseases. The aim of the study was to evaluate fungal protease activity during cytokine production in nasal polyp epithelial cells and to determine the expression of Toll-like receptor (TLR) mRNA by fungi. Methods: Nasal polyp epithelial cells were obtained from patients and stimulated with Alternaria and Aspergillus. Interleukin-8 (IL-8) and granulocyte macrophage colony-stimulating factor (GM-CSF) were measured to determine the activation of epithelial cells. Reverse transcriptase polymerase chain reaction for the TLR mRNA expression of the nasal epithelial cells was performed. Cytokine production was inhibited with protease inhibitors and anti-human TLR antibodies. Results: The fungi enhanced the production of IL-8 and GM-CSF from nasal epithelial cells. When nasal epithelial cells were activated by the fungi, TLR2, TLR3 and TLR4 mRNAs were more strongly expressed than in the nonactivated cells. Cytokine production was inhibited by protease inhibitors and anti-human TLR4 antibodies. Conclusions: The results of this study showed that fungi interacted with nasal epithelial cells and enhanced the production of cytokines and TLR mRNA expression. The cytokine production was related to the protease in fungi and TLR4.

Silver has long been known as a strong antimicrobial and disinfectant. Several types of nano-silver coated products have been developed. However, the antimicrobial and disinfectant characteristics of nano-silver have not been well studied. The aim of this study was to investigate the effect of nano-silver on allergic inflammation in a mouse model. Female BALB/C mice were sensitized by intraperitoneal injection of ovalbumin (OVA) and aluminium hydroxide on days 0, 7, 14, and 21. Mice were challenged with intranasal instillation of OVA. Nano-silver was also administered nasally prior to intranasal instillation of OVA. Severity of allergic rhinitis was assessed according to nasal symptoms, serum OVA-specific IgE level, interleukin (IL)-4, IL-10, and interferon (INF)-γ levels in nasal lavage fluid. Hematoxylin-eosin stain and periodic acid-Schiff stain were performed for evaluation of histological change. Nano-silver attenuated manifestation of nasal symptoms in sensitized mice and inhibited production of OVA-specific IgE, IL-4, and IL-10, however, it had no effect on INF-γ level. In addition, the degree of inflammatory cell infiltration and goblet cell hyperplasia was attenuated by nano-silver. These results suggest that nano-silver may effectively reduce allergic inflammation in a mouse model of allergic rhinitis. Through its properties as an anti-inflammatory agent, nano-silver may be a useful therapeutic strategy.