E-cigarette use is rapidly increasing worldwide, yet there is limited research into the effects of vaping on susceptibility to respiratory infection. Evidence shows that vulnerability to invasive pneumococcal disease is associated with exposure to tobacco smoke [1]. Bacterial adherence to host cells is key to colonisation and infection. A mechanism by which pneumococci adhere to airway cells is by co-opting host expressed platelet-activating factor receptor (PAFR). We previously reported that PAFR expression is increased by cigarette smoke [1]. In this study, we sought to determine if nasal PAFR expression is increased with E-cigarette use in vivo. Nasal biopsies were taken from E-cigarette users (N=10) before and 1hour after an observed 5-minute vaping session. All individuals used their regular brand of E-cigarette and E-liquid. Nasal cells taken before the vaping session (N=8) were also exposed to 24mg/ml nicotine (N+) E-cigarette vapour (ECV) in vitro for 2.5 hours. Nasal epithelial PAFR expression was subsequently assessed by flow cytometry. A significant increase in nasal PAFR expression was observed in participants post E-cigarette use (p<0.05) (figure 1a). A significant increase in PAFR expression was also observed in nasal cells from participants that were exposed to 24mg/ml nicotine ECV in vitro (p<0.01) (figure 1b). Data are expressed as median fluorescence intensity (MFI) adjusting for isotypic control and analysed by paired t-test. This study provides preliminary evidence that nasal epithelial PAFR expression, as with conventional tobacco, is increased by E-cigarette vapour. In vitro studies suggest that this is in part due to nicotine. We speculate that increased PAFR expression in E-cigarette exposed airway cells increases vulnerability to pneumococcal infection.