Claudin-18 deficiency is associated with airway epithelial barrier dysfunction and asthma.

ABSTRACT:

Background

Epithelial barrier dysfunction and increased permeability may contribute to antigen sensitization and disease progression in asthma. Claudin-18.1 is the only known lung-specific tight junction protein, but its contribution to airway barrier function or asthma is unclear.

Objectives

We sought to test the hypotheses that claudin-18 is a determinant of airway epithelial barrier function that is downregulated by IL-13 and that claudin-18 deficiency results in increased aeroantigen sensitization and airway hyperresponsiveness.

Methods

Claudin-18.1 mRNA levels were measured in airway epithelial brushings from healthy controls and patients with asthma. In patients with asthma, claudin-18 levels were compared with a three-gene-mean marker of T_H2 inflamma

SUBMITTER: Sweerus K 

PROVIDER: S-EPMC5073041 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature