Establish possible endotypes in patients diagnosed with CRSwNP in the case of primary and recurrent nasal polyps by determining tissue cytokines, proliferation markers and antimicrobial proteins. Material obtained from 8 patients was divided into 4 cases with recurrent polyps and 4 primary ones. Samples of polyps were taken during nasal surgery. Controls were 17 tissue samples of healthy nasal mucosa. Immunohistochemical analysis was performed to detect Ki-67, β-Defensin 2, IL-1, IL-4, IL-6, IL-7, IL-8, IL-10, IL-12. Results were determined semi-quantitatively and evaluated with the use of Mann-Whitney U test and Spearman’s rank correlation. Number of positive structures in Ki-67 (p=0.006), β-Defensin 2 (p=0.002), IL-1, IL-4, IL-6, IL-8, IL-10, IL-12 (p<0.001) was significantly increased in connective tissue of nasal polyps. Immunoreactive cells of β-Defensin 2, IL-4, IL-6, IL-7, IL-8, IL-10, IL-12 (p<0.001) were significantly decreased in superficial epithelium of nasal polyps. There were no significant differences in cytokine and antimicrobial peptide expression between primary and recurrent patient groups. There was a strong positive correlation between number of β-Defensin 2 and connective tissue IL-8; connective tissue IL-1 and both connective tissue and epithelial IL-4; connective tissue IL-4 and epithelial IL-4; epithelial IL-6 and IL-8 in primary polyps. Recurrent polyps demonstrated a strong negative correlation between IL-1 and both epithelial IL-1 and IL-10; IL-6 and IL-10 as well as a strong positive correlation between epithelial IL-1 and IL-10; epithelial IL-7 and IL8. Increase in cytokine and antimicrobial peptide appearance in the connective tissue and a decrease in the epithelium of a nasal polyp indicates a significant intensification of the connective tissue immune response and stimulation of immune cell differentiation. Difference in correlating factors as well as emerging negative correlations could indicate a dysregulation of cytokine secretion in recurrent CRSwNP as the disease progresses.
- 3.4. Other publications in conference proceedings (including local)