Electronic cigarettes or vaping products have been marketed as a safer alternative to smoking, but very little is known about the health effects in the human lung, particularly in the distal airways, a key site of
airway obstruction and destruction in
chronic obstructive pulmonary disease that is often exacerbated by
viral infections. The aim of this study was to investigate the effects of
electronic cigarette vapor (e-vapor) on human distal airway epithelial responses to influenza A virus (IAV)
infection. We isolated primary small airway epithelial cells (SAECs) from donor lungs free of
lung disease, and cultured them at air-liquid interface (ALI). To measure markers of epithelial injury such as integrity of epithelial barrier structure and function, we selected a regimen of non-toxic, barrier preserving e-vapor exposure of cultured cells to 15 puffs of e-vapor from a commercially available e-cigarette once per day for 3 days, prior to IAV
infection. After 72 h of
infection, media and cell lysates were collected to measure
cytokines involved in inflammatory and
antiviral responses. Pre-exposure to e-vapor with IAV
infection, compared to IAV
infection alone, significantly increased inflammatory and
antiviral mediators including
IL-8, CXCL10, IFN-beta, and MX1. Our results suggest that e-vapor exposure amplifies human distal airway pro-inflammatory response to IAV
infection, independently of the severity of cell injury during
viral infection.