# Role of Periostin in the Development of Nasal Hyperresponsiveness in Mice with Allergic Rhinitis

## TL;DR

This study shows that Periostin, a protein linked to inflammation, contributes to nasal hyperresponsiveness in a mouse model of allergic rhinitis.

## Contribution

The study demonstrates that Periostin directly causes nasal hyperresponsiveness in allergic rhinitis.

## Key findings

- Nasal hyperresponsiveness in AR mice is associated with increased Periostin gene expression.
- Recombinant Periostin administered to healthy mice induces nasal hyperresponsiveness.
- Integrin subunits αV, β3, and β5 are expressed in nasal mucosa, suggesting a receptor role for Periostin.

## Abstract

Periostin is a matricellular protein induced by type 2 cytokines. It has been shown to play important roles in airway inflammation and tissue remodeling. Although periostin has been studied in asthma and chronic rhinosinusitis, its role in allergic rhinitis (AR) and nasal hyperresponsiveness (NHR) is unclear. This study aimed to determine whether periostin is involved in the development of NHR in AR. A murine AR model was established by sensitization and repeated intranasal challenges with Japanese cedar pollen (JCP). In this animal model of AR, an increase in nasal responsiveness to histamine was observed 24 h after the last JCP challenge, indicating the development of NHR. RT-qPCR analysis revealed that the JCP-induced NHR was accompanied by increased periostin gene expression. Immunohistochemical examinations demonstrated the expression of integrin subunits αV (Itgav), β3 (Itgb3) and β5 (Itgb5), which are known as receptors for periostin, in the nasal mucosa, especially in the mucosal epithelium. Notably, repeated intranasal administration of recombinant periostin to healthy I mice reproduced the NHR phenotype, as observed in AR model mice. These findings suggest that periostin upregulation in the nasal mucosa plays a causal role in the development of NHR, a key feature of AR.