Airway epithelium is a frontline defense system against environmental insults, such as inhaled cigarette smoke, pollutants and airborne pathogens, which are amongst the primary risk factors for the development of IPF and COPD. A persistent epithelial damage may cause not only structural but also functional alterations, leading to aberrant activation of signalling pathways involved in cell differentiation, wound healing and inflammation.

Here we aimed to systematically examine and compare the effects of a panel of triggers (EGF, IL-13, TNF-?, and TGF-?1, LPA and LPS) in humans (A549, BEAS-2B) and murine (C57BL/6) respiratory epithelial cells in a wound healing assay (WHA or scratch assay).

We performed the WHA in the two-dimensional cell monolayer format. All cell types were cultured to confluence and starved for 24h, and subsequently exposed to the single stimuli after a mechanical simulation, by making a scratch. Wound repair assessment was recorded after 24 and 48h.

All tested cell types displayed distinct patterns of sensitivity to the different stimuli with EGF, LPA, and TNF-? producing the larger and most consistent stimulation of wound healing. A549 cells were also sensitive to TGF-?1, while BEAS-2B was to LPS. Interestingly, IL-13 significantly inhibited wound repair in the three cell types.

The present results may contribute to our understanding of the mechanisms involved in airway wound repair and can be instrumental in the identification of innovative therapeutic targets for IPF and COPD.