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Abstract
Problem: Thymic stromal lymphopoietin (TSLP) produced by epithelial cells is capable of initiating via dendritic cells (CD11c+) a Th2 immune response. The aim of this study was to evaluate the expression of TSLP and Interleukin 5 (IL-5) in nasal mucosa and to discuss their role for chronic hyperplastic rhinosinusitis with nasal polyps (CHS/NP). Methods: Twelve subjects with CHS/NP and 12 subjects undergoing routine surgery for septal deviation without sinusitis (controls) were included in this study. Homogenized mucosal specimens were analyzed by relative quantitative real-time-PCR for the expression of TSLP and IL-5. Allergy screening tests revealed that 5 subjects of CHS/NP were sensitized to aeroallergens. None of the controls had positive allergy screening tests. Results: The tissue expression of TSLP was significantly higher in CHS/NP compared to the control group (ANOVA, P = 0.004). Bonferroni‘s post hoc analyses (CHS/NP with allegy vs CHS/NP without allergy vs controls) revealed significant higher expression levels in both CHS/NP subgroups with and without allergic sensitization than in controls. Interestingly, the factor “sensitization” had no significant effect on the TSLP expression within the CHS/NP group. Whereas IL-5 was expressed in all nasal polyps, it was only detectable in 58% of control nasal mucosa. Furthermore, IL-5 expression in CHS/NP was significantly higher compared to controls (ANOVA, P = 0.002). Correlational analyses revealed that there was a significant relation between TSLP and IL-5 expression (r 24 = 0.65, P = 0.001). Conclusion: In this study we first demonstrated TSLP gene expression in nasal mucosa. TSLP was significantly higher expressed in nasal polyps than in healthy mucosa, supporting the hypothesis that this mediator may play an important role for the inflammation in CHS/NP. Interestingly, TSLP seems to be involved in regulation of IL-5 expression. Significance: In contrast to other cytokines TSLP could be produced by resident nasal epithelial cells, inducing a Th2 immune response at the beginning of the sinus disease. Support: None reported.
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