Effect of the iQOS electronic cigarette device on susceptibility to S. pneumoniae infection
Saturday, March 3, 2018
South Hall A2 (Convention Center)
Lisa Miyashita, PhD, Jonathan Grigg, BSc MB BS MD

Bacterial adherence to host cells is key to infection. A mechanism by which pneumococci adhere to airway cells is by co-opting the platelet-activating factor receptor (PAFR). We previously reported that in vitro PAFR expression is increased by cigarette smoke (1). The popularity of electronic cigarette devises has rapidly increased worldwide and are marketed as a safer alternative to conventional cigarettes. We thus sought to determine if nasal PAFR expression is increased with the use of the most current device on the market, iQOS, a heat-not-burn cigarette device.


iQOS stocks were made by simulating a vaping session using a peristaltic pump at a fixed rate. Primary nasal epithelial cells were exposed to iQOS extract for 2.5 hours before measuring PAFR expression by monoclonal antibody and flow cytometry. Data were expressed as median fluorescent intensity adjusting for isotypic control and analysed by Mann-Whitney. On one occasion, pneumococcal adhesion was measured following iQOS extract exposure by adding the S. pneumoniae strain D39 for a further 2 hours and plating for colony forming units.


Nasal epithelial PAFR expression was significantly increased in cells exposed to iQOS extract (P <0.05). Pneumococcal adhesion to nasal epithelial cells was also observed to increase.


This study provides preliminary evidence that use of a heat-not-burn cigarette device increases vulnerability to airway infection and infection-triggered asthma exacerbations.


(1) Grigg, J., et al., Thorax, 2012. 67 (10): p. 908 - 13.