Abstract
Problem
The pathogenesis of eosinophilic chronic rhino-sinusitis (ECRS) is still unclear. Paranasal mucosa inflammation might be related to eosinophil infiltration. Eosinophil infiltration seems to induce changes in the expression of cell adhesion molecules, such as VCAM-1. Futhermore Mediators such as Interleukin 5 and 13 (IL-5, IL-13) are considered to be key factors for eosinophilic accumulation and activation. The E - Cadherin – β - catenin complex maintain the integrity of epithelium. Down-regulation of β-catenin and E-cadherin is a pivotal factor for loose integrity and progressive cell growth. This study aimed to assess which cytokines regulate the expression of the adhesion molecule E-cadherin and the multifunctional protein β-catenin, playing an essential role in the cadherin-mediated anchoring, in ECRS.
Methods
ECRS cell cultures were incubated with IL-5, IL-13 and VCAM-1 and β-catenin / E-cadherin levels were analysed after 8–72 hours using cytokine immunoassay and immuno-histochemistry.
Results
We could ascertain a significant increase in β-catenin expression in eosinophilic paranasal cell culture after IL-13 administration compared to non-eosinophilic culture. Stimulation with IL-5 did demonstrate an alteration of E-cadherin expression. Incubation with VCAM-1 could induce a significant increase in E-cadherin expression in fibroblast cell cultures. Immuno-staining for β-catenin was restricted to the membrane of the cells.
Conclusion
In regard to the increased mural expression of β-catenin, we presume that a fibrotic reaction similar to asthma and chronic obstructive pulmonary disease is taking place in patients suffering from CRS.
Significance
The tissue remodelling during chronic eosinophilic inflammation offers new insight into pathogenesis of ECRS.
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