Eosinophilic chronic rhinosinusitis (ECRS) is considered a refractory and intractable disease. Patients with ECRS present with thick mucus production, long-term nasal congestion, loss of sense of smell, and intermittent acute exacerbations secondary to bacterial infections. Despite medical and surgical interventions, there is a high rate of recurrence with significant impairment to quality of life. The recent increasing prevalence of ECRS in south Asian countries and the strong tendency of ECRS to reoccur after surgery should be considered. The majority of cases need repeat surgery, and histological examinations of these cases show eosinophilic-dominant inflammation. The degradation and accumulation of eosinophils, release of cytokines, and mucus secretion have important roles in the pathogenesis of ECRS. ECRS differs from non-ECRS, in which eosinophils are not involved in the pathogenesis of the disease, and also in terms of many clinical characteristics, blood examination and nasal polyp histological findings, clinical features of the disease after surgery, efficacy of medications, and computed tomography findings. This review describes the clinical course, diagnosis, and treatment of ECRS as well as its pathophysiology and the role of eosinophils, mucus, cytokines, and other mediators in the pathogenesis of ECRS.

Keywords: biomarker, circulating miRNA, head and neck squamous cell carcinoma, miR-99a, miR-223Abbreviations: HNSCC, head and neck squamous cell carcinoma; miRNA, microRNA.Circulating microRNAs (miRNAs) are emerging as promising non-invasive biomarkers for human cancer. Head and neck squamous cell carcinoma (HNSCC) is a prevalent malignancy worldwide, but its overall survival has remained unchanged in the past 3 decades. Biomarkers for evaluating efficacy of cancer therapy are urgently needed. To explore circulating miRNAs as cancer therapy biomarkers, we initially identified that 8 miRNAs were distinctly dysregulated in cancerous tissues compared with adjacent non-cancerous counterparts from 16 patients, using microarray and realtime PCR. Based on this discovery, the comparison study was performed between pre-and 6 months post-operative paired plasma samples on 9 patients. MiR-99a, which was down-regulated in cancerous tissues, was significantly increased in plasma after operation. Meanwhile, oncomiR miR-21 and miR-223 that were up-regulated in cancerous tissues, were significantly reduced in post-operative plasma samples. We firstly report the significant changes of miR99a in plasma of HNSCC patients after surgery. Furthermore, plasma miR-223 was inversely increased in a patient whose cancer relapsed within 6 months after operation. We conclude that these circulating miRNAs may serve as biomarkers to evaluate the efficacy of therapy and the prognosis of HNSCC.

Prophylactic SLIT is effective for prevention of the development of pollinosis. Induction of IL-10 producing T cells, B cells and monocytes is an important mechanism of SLIT for prevention of pollinosis in asymptomatic but sensitized subjects.

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Background: Interleukin-31 (IL-31) is a newly discovered T helper lymphocyte-derived cytokine that plays an important role in allergic inflammation. However, the effects of IL-31 on mucus production in nasal allergic inflammation are completely unknown. Objective: To investigate the effects of IL-31 on mucin gene expression (MUC5AC) in patients with allergic rhinitis and in human airway epithelial cells. Methods: Expression levels of IL-31 and IL-31 receptor A (IL-31RA) were evaluated in the inferior turbinate of patients with allergic rhinitis and non-allergic rhinitis with immunohistochemistry. IL-31-induced MUC5AC gene expression was measured with a MUC5AC luciferase reporter assay in human epithelial HM3-MUC5AC cells and quantified by quantitative real-time polymerase chain reaction in human airway epithelial A549 cells. Results: IL-31RA was primarily localized in submucosal glands and upregulated in allergic rhinitis. IL-31 was detected in submucosal tissue and increased in allergic inflammation. MUC5AC gene expression was induced by IL-31 stimulation both in HM3-MUC5AC and A549 cells. Additionally, IL-31 cooperated with Th2 cytokines on MUC5AC gene expression in HM3-MUC5AC cells. Conclusion: IL-31 and IL-31RA are upregulated in patients with allergic rhinitis, and induce MUC5AC gene expression in human airway epithelial cells. These findings suggest that IL-31 plays an important role in mucus overproduction in nasal allergic inflammation.