Understanding the mechanisms of epithelial repair provides important insights into airway diseases such as asthma and COPD. The airway epithelial structure differs between the larger conducting airways and bronchioles in which, characteristically, basal cells are absent. In the distal airway Clara cells are absolutely necessary for epithelial repair but this is not so in tracheobronchial tissue. Here, the relative contribution to repair from Clara and basal cells is controversial.

This study explores the role of basal cells as a progenitor population in mouse bronchial epithelium ablated of Clara cells. Basal cells, identified by CK14 and GSI-B₄ immunoreactivity, renewed bronchial epithelium after ganciclovir mediated depletion of Clara cells in CCtk transgenic mice and after naphthalene induced airway injury. Naphthalene is a toxin which specifically targets Clara cells. Following injury, basal cells were proliferative and adopted an intermediate morphology and molecular phenotype between true basal and Clara cells. In addition, the multipotential differentiation capacity of these cells was confirmed by an elegant lineage analysis in bitransgenic K14/RS mice in which basal, Clara, and ciliated cell populations were found to have arisen from CK14 expressing progenitors.

The authors have used multiple methodologies to establish the stem cell niche of epithelial basal cells in the mouse bronchus, providing evidence that they function as a transient amplifying cell in response to injury. If applicable to humans, this work implicates bronchial basal cells as contributory to the pathobiology of chronic lung diseases, and renders these cells as possible therapeutic targets. Bronchial basal cells are a worthy focus of further translational research.