Silencing of &amp;lt;i&amp;gt;ERK2&amp;lt;/i&amp;gt; with Small Interference RNA Regulates the Expression of CXCL1 in Th17 Cell

Wei Wu,Hui Chen,Kaixia Cai,Dan Wang,Qian Zhang

doi:10.4236/jbm.2021.97017

Abstract

Patients with steroid-resistant asthma had their monocyte-derived TH17 cells collected. The expression levels of ERK2 in the TH17 were silenced and inhibited using ERK2 specific small interfering RNA (siRNA). By screening of CXCL1 and IL-17A in the TH17 culture supernatant, the expression levels of ERK2 and CXCL1 were determined. Using targeted siRNA to inhibit ERK2, the expression of ERK2 in the TH17 was reduced. Furthermore, inhibiting ERK2 hindered CXCL1 expression and decreased CXCL1 and IL-17A production. These findings suggest that ERK2 is involved in the synthesis of CXCL1 and IL-17A, two proteins that play a key role in the pathogenesis of hormone-resistant asthma.

Highlights

Asthma is a common chronic respiratory disease, and its global incidence is increasing year by year
Inhibiting ERK2 hindered CXCL1 expression and decreased CXCL1 and IL-17A production. These findings suggest that ERK2 is involved in the synthesis of CXCL1 and IL-17A, two proteins that play a key role in the pathogenesis of hormone-resistant asthma
This study aimed to explore the molecular mechanisms of adhesion molecule CXCL1 and the Raf-ERK signaling pathways in Th17 cell-mediated neutrophil airway infiltration, thereby deepening the understanding of hormone-resistant asthma

Summary

Introduction

Asthma is a common chronic respiratory disease, and its global incidence is increasing year by year. Symptoms persist in about 5% - 10% of asthma patients who have received adequate glucocorticoid therapy These patients remain in a poorly controlled state and are affected by hormoneinsensitive or hormone-resistant asthma, subjecting the patient to greater physiological and psychological impact [3]. Airway infiltration with neutrophils as the primary inflammatory cells is the main pathophysiological basis of hormone-resistant asthma. This phenomenon is closely related to a new class of helper Tlymphocytes, namely, Th17 cells. This study aimed to explore the molecular mechanisms of adhesion molecule CXCL1 and the Raf-ERK signaling pathways in Th17 cell-mediated neutrophil airway infiltration, thereby deepening the understanding of hormone-resistant asthma

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