Interleukin (IL)-17A is a highly inflammatory cytokine and is known to be produced by Th17 cells. The importance of IL-17A expression in nasal epithelial cells is not well understood. The goal of this study is to explore the expression of IL-17A in nasal epithelial cells in vivo and in vitro. IL-17A and staphylococcal enterotoxin B (SEB) were detected by immunofluorescence (IF) in nasal epithelial cells of control mucosa (n = 10) and nasal polyps (n = 20). Expression of IL-17A, RORC, IL-6, and TGF-β1 was also measured by RT-PCR in the tissue of control nasal mucosa (n = 10) and nasal polyps (n = 20). IL-17A expression was evaluated in the human nasal epithelial cells after SEB stimulation. Finally, IL-17A expression was demonstrated by immunohistochemistry and IF following intranasal SEB instillation in mice. Expression of IL-17A in nasal epithelial cells was higher in nasal polyps compared to control mucosa. There was a significant correlation between IL-17A and SEB detection in nasal polyps using IF. SEB increased IL-17A expression in human nasal epithelial cells, and in epithelial cells of SEB instilled mice. In conclusion, SEB exposure of nasal epithelial cells induces the enhanced expression of IL-17A. SEB may be involved in pathogenesis of nasal polyps by enhancing IL-17A expression in epithelial cells in nasal polyps.

To investigate the incidence and severity of pulmonary function impairment in patients with chronic rhinosinusitis with nasal polyps (CRSwNP).In this prospective study, fifty-six patients with bilateral CRSwNP who were scheduled for functional endoscopic sinus surgery during a period from March to June 2010 in the Department of Otolaryngology of Qilu Hospital, were recruited in this study. Routine medical and rhinological examinations such as nasal endoscopy, sinus CT scan, and skin prick tests (SPT) for common inhalant and food allergens, and cytological examination of the paraffin-embedded NP tissues were performed together with a full assessment of the pulmonary functions.Based on the pulmonary function tests, the rate of patients showing bronchial hyperresponsiveness (BHR), asthma, and abnormal pulmonery functions were 37.5%, 44.6%, and 53.6%. In patients who did not have a history of lower airway symptoms, the rate of abnormal pulmonary functions was 50.0%, the rate of BHR was 43.2%. There was an increased rate of BHR, asthma and abnormal pulmonary functions in patients with a higher polyp grading score or Lund Mackay CT scan score (polyp grading score: χ(2) were 8.077, 3.989 and 7.445, P < 0.01 or < 0.05. CT scan score: χ(2) were 3.863, 5.380 and 4.309; 4.293, 4.293 and 4.572; 10.572, 13.504 and 13.295, P < 0.01 or < 0.05). The rate of BHR and asthma in patients with positive SPT were higher (P < 0.05). In patients with eosinophils hyperplasia in nasal polyps, the rate of BHR, asthma and abnormal pulmonary functions were higher (χ(2) were 4.065, 5.217 and 3.376, P < 0.05 or P < 0.01).There is a high risk of developing lower airway diseases in patients with CRSwNP.

BACKGROUND:

Since the recent establishment of a murine model of eosinophilic chronic rhinosinusitis with nasal polyps (CRSwNP), both the development of new drugs for treatment or prevention of eosinophilic CRSwNP and elucidation of their pathogenesis have been feasible. We investigated the therapeutic effects of resveratrol on CRSwNP and its mechanism of action using a murine model.

METHODS:

After induction of eosinophilic CRSwNP, the therapeutic effects of resveratrol were tested and compared with those of triamcinolone acetonide. Histopathologic changes were evaluated using hematoxylin and eosin for overall inflammation, Sirius red for eosinophils, and Masson's trichrome stain for collagen. The expression levels of the interleukin (IL)-4, IL-5, prostaglandin D synthase, and leukotriene C4 synthase genes were assessed by quantitative real-time PCR. Cyclooxygense-2 and 5-lipoxygense levels were evaluated by immunohistochemical staining and Western blot analysis.

RESULTS:

The degree of eosinophilic infiltration and subepithelial fibrosis was significantly decreased by administration of high-dose resveratrol, the potency of which was similar to that of triamcinolone acetonide. The expression levels of the IL-4, IL-5, prostaglandin D synthase, and leukotriene C4 synthase genes were significantly decreased by administration of low- or high-dose resveratrol. The production of 5-lipoxygenase was strongly inhibited by high-dose resveratrol.

CONCLUSIONS:

Resveratrol may be useful for the prevention of eosinophilic CRSwNP. A key mechanism of its action is believed to be its anti-inflammatory effect, particularly on eosinophils, by inhibiting the lipoxygenase pathway.

Chronic rhinosinusitis (CRS) significantly affects patient quality of life. Medical and surgical treatments aim to clinically manage the condition.

OBJECTIVE:

To assess the long-term quality of life and clinical management of CRS in patients submitted to endoscopic sinus surgery.

METHOD:

This prospective cross-sectional cohort study enrolled 38 patients and looked into the follow-up data of subjects diagnosed with CRS before surgery, three months after surgery, and at least two years after surgery. The Sinonasal Outcome Test 22 (SNOT-22) was used to assess response to treatment and long-term clinical management of the disease.

RESULTS:

Significant improvements in the SNOT-22 scores were seen between the preoperative (61.3) and postoperative assessments with three (16.9) and 24 (32.3) months. No statistically significant differences were seen when patients with polyps were compared to polyp-free subjects. Few patients were controlled in both groups, and 7.89% of the subjects had revision surgery during the study.

CONCLUSION:

Endoscopic sinus surgery significantly improved the quality of life of patients with chronic rhinosinusitis. Clinical control of the condition was acceptable, with few patients requiring re-operation within two years of the first surgery.

The aim of the present study was to investigate the expression, distribution and function of dendritic cells (DCs) and to study their role in nasal polyps. The study involved 55 participants, 45 of whom had nasal polyps and were the study group and 10 who had normal inferior turbinates and were the control group. Immunohistochemical staining was used to visualize the expression and distribution of the S-100 protein. A double immunostaining method was used to visualize the CD1a and CD40 expression and the images were analyzed with Axioplan 2 microscopy. The expression level of the S-100 protein in the nasal polyps was higher than that in the normal inferior turbinates with a significant difference (P<0.01). The distribution area, number and density of the double stained cells in the nasal polyps were all greater than in the normal inferior turbinates (P<0.01). The S-100 protein and double stained cells were mainly located in the lamina propria below the mucous membrane. The present study demonstrates that DCs are involved in the pathogenesis of nasal polyps and the presence of CD40-positive DCs suggests that this was related to the reciprocal interaction between the DCs and T lymphocytes.

To detect the expression and distribution of the lung surfactant protein D (surfactant protein D,SP-D ) and IL-16 in nasal mucosa of allergic rhinitis and nasal polyps, and then probe into their significance in the pathology of allergic rhinitis and nasal polyps.Fifteen cases of allergic rhinitis, fifteen cases of nasal polyps and fifteen cases of inferior turbinate mucosa were studied to detect the expression of SP-D and IL-16 by immunohistochemistry method.The expression of SP-D and IL-16 in allergic rhinitis and nasal polyps were dramatically higher in controls (P < 0.01). There was no remarkable difference in the expression of SP-D and IL-16 between allergic rhinitis and nasal polyps (P > 0.05).Both normal tissue and diseased tissue express SP-D and IL-16. SP-D is likely to play key roles in the inflammatory reaction process of allergic rhinitis and nasal polyps. IL-16 is an important eosinophil chemokine in the process of allergic rhinitis and nasal polyps,and it can also enhance the local role of eosinophils,thus it can involve in the process of allergic rhinitis and nasal polyps disease.

Background:

Total and specific immunoglobulin E (IgE) in nasal polyps (NP) is related to local eosinophilic inflammation. However, it remains unclear which antigens cause a stronger accumulation of eosinophils in NP. We investigated whether local IgEs to specific antigens correlated with local eosinophil accumulation.

Methods:

Total IgE, antigen-specific IgEs [5 species of fungi, staphylococcal enterotoxins A and B (SEA and SEB), cedar pollen, ragweed pollen and house-dust mites] and eosinophil cationic protein (ECP) were measured in sinus mucosa homogenates and serum from 29 patients with chronic rhinosinusitis with NP (CRSwNP), 8 patients with allergic fungal rhinosinusitis (AFRS) and 8 control subjects without CRS. The level of ECP in NP was analyzed for correlations with the total and specific IgE levels in the serum and NP.

Results:

In CRSwNP, antigen-specific IgEs [Alternaria > mite (Dp) > Aspergillus > SEB > Penicillium > mite (Df), but not the other fungi, SEA or pollens] in the sinus mucosa correlated significantly with the local ECP. In AFRS, antigen-specific IgEs [Penicillium > mite (Df) > Alternaria, but not the other fungi, SEs or pollens] in the sinus mucosa correlated significantly with the local ECP.

Conclusions:

Local total IgE and antigen (fungi, mites and SEs)-specific IgEs in NP are related to the local eosinophilic inflammation of AFRS and CRSwNP.

The contributing role of specific IgE sensitization in the pathophysiology of sinonasal diseases including rhinitis, chronic rhinosinusitis (CRS), and nasal polyps is explored. Although it is estimated that sensitization to environmental allergens is present in 75% of patients with rhinitis, the role of allergy in CRS and nasal polyps is less certain. However, when atopy is present in the setting of nasal polyps, it is associated with worse quality of life and a higher incidence of asthma. Several theories have been put forth whereby inhalant aeroallergen exposure could drive the inflammatory response that occurs both in the nose and in the sinuses. Tools available to determine the presence of allergic sensitization include skin tests for immediate hypersensitivity, in vitro testing for allergen-specific IgE, and nasal allergen provocation testing. Whether by skin testing or in vitro testing, the identification of specific IgE requires clinical correlation with the history and physical exam.