# EGFR inhibitors suppress house dust mite allergen Der pII induced inflammation in monocytes and macrophages

## TL;DR

This study shows that EGFR inhibitors can reduce inflammation caused by house dust mite allergens in immune cells, suggesting a new treatment approach for allergic asthma.

## Contribution

The novel contribution is demonstrating that EGFR inhibitors suppress Der pII-induced inflammation in monocytes and macrophages.

## Key findings

- Der pII induces IL-6, IL-8, and TNF-α in immune cells.
- EGFR inhibitors reduce IL-6 and IL-8 secretion in these cells.
- AZD-9291 inhibits NO production in alveolar macrophages.

## Abstract

Allergic asthma, often triggered by house dust mites (HDMs), is characterized by airway inflammation, mucus hypersecretion, and airway hyperresponsiveness. Among the major HDM allergens, Der pII plays a significant role in promoting inflammation. This study investigates the role of epidermal growth factor receptor (EGFR) inhibitors in modulating Der pII-induced cytokine production and inflammation in human immune cells.

Recombinant GST-Der pII protein was expressed and purified for subsequent studies. Human peripheral blood mononuclear cells (HPBMC), THP-1 monocytes, THP-1-derived macrophages, and pulmonary alveolar macrophages (NR8383) were exposed to Der pII, followed by treatment with EGFR inhibitors AZD-9291 and Tarceva. Enzyme-linked immunosorbent assay (ELISA) was used to detect the expressions of IL-6 and IL-8. Nitric oxide (NO) levels were determined using the Griess Reagent System.

Der pII significantly induced pro-inflammatory cytokines, including IL-6, IL-8, and TNF-α in HPBMC and THP-1 cells. Both EGFR inhibitors reduced the secretion of IL-6 and IL-8 in these cell types. In THP-1 macrophages, AZD-9291 suppressed IL-6 expression and CD14/CD36 macrophage markers. Moreover, AZD-9291 significantly inhibited NO production in alveolar macrophages.

These findings suggest that EGFR plays a critical role in mediating Der pII-induced inflammation, and EGFR inhibitors may represent a potential therapeutic approach for controlling HDM-induced allergic inflammation.