Epithelial Aryl Hydrocarbon Receptor Protects From Mucus Production by Inhibiting ROS-Triggered NLRP3 Inflammasome in Asthma.

ABSTRACT:

Background

Despite long-standing recognition in the significance of mucus overproduction in asthma, its etiology remains poorly understood. Muc5ac is a secretory mucin that has been associated with reduced pulmonary function and asthma exacerbations.

Objectives

We sought to investigate the immunological pathway that controls Muc5ac expression and allergic airway inflammation in asthma.

Methods

Cockroach allergen-induced Muc5ac expression and aryl hydrocarbon receptor (AhR) signaling activation was examined in the human bronchial epithelial cells (HBECs) and mouse model of asthma. AhR regulation of Muc5ac expression, mitochondrial ROS (Mito-ROS) generation, and NLRP3 inflammasome was determined by AhR knockdown, the antagonist CH223191, and AhR^-/- mice. The

SUBMITTER: Hu X 

PROVIDER: S-EPMC8634667 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature