Background: IL‐31, a recently discovered member of the gp130/IL‐6 cytokine family, is mainly expressed by human mast cells and T helper type 2 cells. IL‐31 is a key trigger of atopic dermatitis. Recent studies also suggest a role of IL‐31 in the pathogenesis of other allergic diseases including allergic rhinitis. In the present study we studied the release of IL‐31 and IL‐13 in allergen‐challenged allergic rhinitis patients.Methods: Seven seasonal allergic volunteers underwent unilateral nasal provocation with allergen (and a control challenge) with the disc method out of the allergy season. Nasal symptom scores (rhinorrhea, itching, sneezing, obstruction) and bilateral nasal secretions were quantified before and after allergen provocation. IL‐13 and IL‐31 in nasal secretions and serum were measured by electrochemiluminescent immunoassay or ELISA, respectively.Results: Nasal allergen challenge induced the typical clinical symptoms and physiological changes. IL‐31 and IL‐13 in nasal secretions increased in four and five, respectively, volunteers at 5 h after allergen but not after control challenge. We observed correlation trends between nasal IL‐31 concentrations and IL‐13 concentrations (r = 0.9, p = 0.002), and IL‐31 contents and symptom scores (r = 0.9, p = 0.013) 5 h after allergen provocation. No IL‐31 could be detected contralaterally or systemically in the sera.Conclusions: The observed local upregulation of IL‐31 mainly during the late phase reaction after nasal allergen challenge suggests a role of IL‐31 in allergic rhinitis. In which way IL‐31 modulates the inflammatory reaction and type 2 responses in allergic rhinitis remains to be investigated.

Few diagnostic and prognostic biomarkers are available for head-and-neck squamous cell carcinoma (HNSCC). Long non-coding RNAs (lncRNAs) have shown promise as biomarkers in other cancer types and in some cases functionally contribute to tumor development and progression. Here, we searched for lncRNAs useful as biomarkers in HNSCC. Public datasets were mined for lncRNA candidates. Two independent HNSCC tissue sets and a bladder cancer tissue set were analyzed by RT-qPCR. Effects of lncRNA overexpression or downregulation on cell proliferation, clonogenicity, migration and chemosensitivity were studied in HNSCC cell lines. Data mining revealed prominently CASC9, a lncRNA significantly overexpressed in HNSCC tumor tissues according to the TCGA RNAseq data. Overexpression was confirmed by RT-qPCR analyses of patient tissues from two independent cohorts. CASC9 expression discriminated tumors from normal tissues with even higher specificity than HOTAIR, a lncRNA previously suggested as an HNSCC biomarker. Specificity of HNSCC detection by CASC9 was further improved by combination with HOTAIR. Analysis of TCGA pan-cancer data revealed significant overexpression of CASC9 across different other entities including bladder, liver, lung and stomach cancers and especially in squamous cell carcinoma (SCC) of the lung. By RT-qPCR analysis we furthermore detected stronger CASC9 overexpression in pure SCC of the urinary bladder and mixed urothelial carcinoma with squamous differentiation than in pure urothelial carcinomas. Thus, CASC9 might represent a general diagnostic biomarker and particularly for SCCs. Unexpectedly, up- or downregulation of CASC9 expression in HNSCC cell lines with low or high CASC9 expression, respectively, did not result in significant changes of cell viability, clonogenicity, migration or chemosensitivity. CASC9 is a promising biomarker for HNSCC detection. While regularly overexpressed, however, this lncRNA does not seem to act as a major driver of development or progression in this tumor.