# Therapeutic potential of the topical recombinant human interleukin-1 receptor antagonist in guinea pigs with allergic rhinitis

## TL;DR

This study shows that a recombinant human interleukin-1 receptor antagonist reduces symptoms of allergic rhinitis in guinea pigs.

## Contribution

The study demonstrates the therapeutic potential of rhIL-1Ra for allergic rhinitis in an animal model.

## Key findings

- rhIL-1Ra significantly reduced sneezing and nose rubbing in guinea pigs with allergic rhinitis.
- rhIL-1Ra lowered IgE and IL-1β levels and improved nasal tissue inflammation in treated animals.
- rhIL-1Ra showed comparable efficacy to budesonide in alleviating allergic rhinitis symptoms.

## Abstract

Recombinant human Interleukin receptor antagonist (rhIL-Ra) can bind to the IL-1 receptor on the cell membrane and reversibly blocks the proinflammatory signaling pathway. However, its effect on allergic rhinitis (AR) and the underlying mechanism remains unknown. This study aims to investigate the efficacy of recombinant human interleukin-1 receptor antagonist (rhIL-1Ra) on AR guinea pigs.

Guinea pigs were systemically sensitized by intraperitoneal injection and topical intranasal instillation with ovalbumin within 21 days. Animals administrated with saline served as the normal control. The AR animals were randomly divided into the model group and distinct concentrations of rhIL-1Ra and budesonide treatment groups. IL-1β and ovalbumin specific IgE levels were detected by ELISA kits. Nasal mucosa tissues were stained with hematoxylin & eosin (HE) for histological examination.

It was found that the numbers of sneezing and nose rubbing were remarkably reduced in rhIL-1Ra and budesonide-treated guinea pigs. Besides, rhIL-1Ra distinctly alleviated IgE levels in serum and IL-1β levels in nasal mucus, together with decreased exfoliation of epithelial cells, eosinophilic infiltration, tissue edema and vascular dilatation.

rhIL-1Ra is effective in AR guinea pigs and may provide a novel potential choice for AR treatments.