Significance of Interleukin-17a and Interleukin-23 in Chronic Rhinosinusitis with Nasal Polyps Rahime Koca1, Mete Eyigor2, Ustun Osma1, Hulya Eyigor2, Mustafa Deniz Yilmaz1, Omer Tarik Selcuk1, Levent Renda1,

Chronic rhinosinusitis (CRS) is a multifactorial disease; however, the presence of nasal polyposis may be a significant underlying etiological factor affecting the pathophysiology. In the pathophysiology of nasal polyposis, up-regulation of adhesion molecules is induced by interleukin-1 (IL-1) in the vascular endothelium and by IL-8 in epithelial cells and neutrophils. This occurs in addition to effusion, which happens as a result of increased secretion of neutrophil chemoattractants and the accumulation of neutrophils. Histomorphological analysis of CRC with nasal polyposis (CRSwNP) has revealed eosinophils and mixed mononuclear cells with a suppression of neutrophil activity. IL-17A is a member of the IL-17 cytokine family, which consists of six cytokines, termed IL17A-F. IL-17A and IL-17F have the highest degree of homology, and IL-17A is also produced in natural killer (NK) cells, neutrophils, eosinophils, and δγT cells. IL-17 is important in host responses to infections and in the regulation the neutrophil response and is significant in the pathogenesis of CRSwNP. Acta Medica Mediterranea, 2017, 33: 211