Oxidised IL-33 drives COPD epithelial pathogenesis via ST2-independent RAGE/EGFR signalling complex.

ABSTRACT:

Background

Epithelial damage, repair and remodelling are critical features of chronic airway diseases including chronic obstructive pulmonary disease (COPD). Interleukin (IL)-33 released from damaged airway epithelia causes inflammation via its receptor, serum stimulation-2 (ST2). Oxidation of IL-33 to a non-ST2-binding form (IL-33^ox) is thought to limit its activity. We investigated whether IL-33^ox has functional activities that are independent of ST2 in the airway epithelium.

Methods

In vitro epithelial damage assays and three-dimensional, air-liquid interface (ALI) cell culture models of healthy and COPD epithelia were used to elucidate the functional role of IL-33^ox. Transcriptomic changes occurring in healthy ALI cultures t

SUBMITTER: Strickson S 

PROVIDER: S-EPMC10533947 | biostudies-literature | 2023 Sep

REPOSITORIES: biostudies-literature