The article was published on Journal of Allergy and Clinical Immunology in March 2019. The authors Bing Yan et al (Beijing TongRen 10 Hospital, Capital Medical University, Beijing) find that CST1 derived from epithelial cells regulates the activation and recruitment of eosinophils, and CST1 expression is regulated by TH2 and TH17 cytokines.
Background & Aims & Conclusions
Chronic rhinosinusitis (CRS) is an inflammatory disease. Studies have shown that the interaction between epithelial cells and immune cells plays a key role in the pathogenesis of chronic sinusitis with nasal polyps (CRSwNP). But the mechanism/s underlying TH-biased inflammation in this process is/are largely unknown.
In this article, the researchers investigate the expression and role of CST1 in modulating eosinophilic inflammation in CRSwNP.
The expression, localization and concentration of CST1 mRNA in nasal tissues of ECRSwNPs, non-ECRSwNPs and controls were detected. The role of this molecule in nasal polyp cells and eosinophils isolated from nasal polyps and peripheral blood was explored.
The results shows that CST1 was mainly expressed by epithelial cells. Compared with the control group, CST1 was significantly increased in ECRSwNP, but decreased in nonECRSwNP. In both ECRSwNP and non-ECRSwNP tissues, CST1 was induced by IL-4 and IL-13. In non-ECRSwNP in the presence of neutrophils, CST1 is inhibited by IL-17A. Epithelium-derived CST1 enhanced eosinophil activation and recruitment by induction of interleukin-5 (IL-5).
