Mechanisms and therapeutic potential of epithelial-immune crosstalk in airway inflammation.

INTRODUCTION

Chronic airway inflammatory diseases mainly comprise chronic rhinosinusitis (CRS), allergic rhinitis (AR), asthma, cystic fibrosis (CF), and chronic obstructive pulmonary disease (COPD). Epithelial cells fulfill a protective role as a barrier; however, when stimulated, these cells also release a variety of cytokines that attract and activate immune cells, including macrophages, neutrophils, and T-lymphocytes. Excessive activation and aggregation of immune cells disrupts the balance of the cellular microenvironment, and leads to impaired immune defense of the airway mucosa, which can further exacerbate an inflammatory response.

AREAS COVERED: In this article, we discuss the key cytokines and immune pathways involved in epithelial-immune cell interactions, and we detail discoveries in the emerging field of single-cell sequencing and summarize monoclonal antibody-targeted therapies. A comprehensive search was conducted using the search terms 'epithelial cell,' 'immune,' 'interaction,' 'cytokines,' 'asthma,' 'chronic sinusitis,' 'allergic rhinitis,' 'monoclonal antibodies,' and 'single-cell sequencing' by querying Google Scholar and PubMed.

EXPERT OPINION: The intricate pathophysiology of airway inflammation remains to be fully elucidated. Emerging technologies, such as single-cell sequencing, have led to a more comprehensive characterization of the immune mechanisms underlying the pathophysiology of airway inflammatory diseases, which points the way to further precision medicine in the future.