Phosphoinositide 3-kinase-delta could be a biomarker for eosinophilic nasal polyps

Abstract

Nasal polyps (NP) cause diverse clinical symptoms of chronic rhinosinusitis (CRS). Chronic inflammation of sinonasal mucosa is known to be crucial in NP formation. We aimed to define the implications of phosphoinositide 3-kinase (PI3K)-δ in nasal inflammation associated with NP by analyzing NP tissue obtained from CRS patients. Results showed that expression of p110δ, a regulatory subunit of PI3K-δ, in NP tissue was increased compared to control tissue. Increased p110δ expression was closely correlated with more severe CRS features. Interestingly, p110δ expression was increased in eosinophilic NP, which are closely related to more complicated clinical courses of the disease. Furthermore, CRS patients possessing NP with higher p110δ expression displayed more eosinophils in NP tissue and blood, higher levels of IL-5 in NP tissue, and more severe features of the disease. Therefore, PI3K-δ may contribute to the formation of NP, especially eosinophilic NP associated with more severe clinical presentations and radiological features.

The role of autophagy regulated by the PI3K/AKT/mTOR pathway and innate lymphoid cells in eosinophilic chronic sinusitis with nasal polyps

“…Kim et al found that PI3k-110δ was increased in eCRSwNP. 9 In this study, we used the eCRSwNP mouse model, PI3K/Akt/mTOR pathway inhibitors, and autophagy inhibitors and activators to investigate the regulatory effects of the PI3K/Akt/mTOR pathway on autophagy, and their effects on eosinophilic inflammation, and tissue remodeling. The role of type 2 innate lymphoid cells (ILC2s) in eCRSwNP was also studied, and the relationship between ILC2s and autophagy was preliminarily determined.…”

“…Class Ⅲ PI3K and mTOR complex 1 (mTORC1) in the PI3K/Akt/mTOR pathway can regulate autophagy 8 ; however, the PI3K/Akt/mTOR pathway has rarely been studied in eCRSwNP and its role remains unclear. Kim et al found that PI3k‐110δ was increased in eCRSwNP 9 …”