E-cigarette vapour contains free radicals with the potential to induce oxidative stress. Since oxidative stress in airway cells increases platelet-activating factor receptor (PAFR) expression, and PAFR is co-opted by pneumococci to adhere to host cells, we hypothesised that E-cigarette vapour increases pneumococcal adhesion to airway cells.Nasal epithelial PAFR was assessed in non-vaping controls, and in adults before and after 5 min of vaping. We determined the effect of vapour on oxidative stress-induced, PAFR-dependent pneumococcal adhesion to airway epithelial cells , and on pneumococcal colonisation in the mouse nasopharynx. Elemental analysis of vapour was done by mass spectrometry, and oxidative potential of vapour assessed by antioxidant depletionThere was no difference in baseline nasal epithelial PAFR expression between vapers (n=11) and controls (n=6). Vaping increased nasal PAFR expression. Nicotine-containing and nicotine-free E-cigarette vapour increased pneumococcal adhesion to airway cells Vapour-stimulated adhesion was attenuated by the PAFR blocker CV3988. Nicotine-containing E-cigarette vapour increased mouse nasal PAFR expression, and nasopharyngeal pneumococcal colonisation. Vapour contained redox-active metals, had considerable oxidative activity, and adhesion was attenuated by the antioxidant N-acetyl cysteine.This study suggests that E-cigarette vapour has the potential to increase susceptibility to pneumococcal infection.

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Background: The World Health Organization estimates that air pollution is responsible for 7 million deaths per annum, with 7% of these attributable to pneumonia. Many of these fatalities have been linked to exposure to high levels of airborne particulates, such as diesel exhaust particles (DEPs). Objectives: We sought to determine whether exposure to DEPs could promote the progression of asymptomatic nasopharyngeal carriage of Streptococcus pneumoniae to invasive pneumococcal disease. Methods: We used mouse models and in vitro assays to provide a mechanistic understanding of the link between DEP exposure and pneumococcal disease risk, and we confirmed our findings by using induced sputum macrophages isolated from healthy human volunteers. Results: We demonstrate that inhaled exposure to DEPs disrupts asymptomatic nasopharyngeal carriage of S pneumoniae in mice, leading to dissemination to lungs and blood. Pneumococci are transported from the nasopharynx to the lungs following exposure to DEPs, leading to increased proinflammatory cytokine production, reduced phagocytic function of alveolar macrophages, and consequently, increased pneumococcal loads within the lungs and translocation into From a the Bacterial Pathogenesis and Immunity Group and d the Microbial Evolution,

Her main research interests investigate the effect of inhaled toxins on respiratory health and susceptibility to respiratory infection, with a particular interest in E-cigarettes or vaping products, and air pollution particulate matter. She is also interested in the effect of inhaled toxins on bacterial virulence properties. She is currently collaborating to define the potentially harmful effects of London Underground-and London traffic-related air pollution particulate matter on respiratory health. Gary Foley is a paediatrician whose main areas of interest include Streptococcus pneumoniae infection, cell surface receptors and air pollution. He is currently conducting a comprehensive study in the paediatric population looking at platelet-activating factor receptor, an immune-related cell surface receptor involved in inflammation that is also a potential gateway for S. pneumoniae infection in children with chronic illness. He is a lecturer at Barts and the London School of Medicine and Dentistry and a Senior Paediatric Registrar in London. He is currently collaborating to define the potentially harmful effects of London Underground-and London traffic-related air pollution particulate matter on respiratory health.