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Background Although the use of e-cigarettes is increasing worldwide, their short and long-term effects remain undefined. We aimed to study the acute effect of short-term use of e-cigarettes containing nicotine on lung function and respiratory symptoms in smokers with airways obstructive disease (COPD, asthma), "healthy" smokers, and healthy never smokers. Methods Respiratory symptoms, vital signs, exhaled NO, airway temperature, airway resistance (Raw), specific airway conductance (sGaw) and single nitrogen breath test were assessed before and immediately after short term use of an e-cigarette containing 11mg of nicotine among adults with COPD, asthma, "healthy" smokers, and never-smokers. The effect of the use of nicotine-free e-cigarettes among "healthy" never smokers was also studied. Results The majority of participants reported acute cough. Short term use of nicotine e-cigarettes was associated: a) with increased heart rate in all subjects except in the COPD group, b) decreased oxygen saturation in "healthy" and COPD smokers, c) increased Raw in asthmatic smokers, "healthy" smokers, and healthy never smokers, d) decreased sGaw in healthy subjects, and e) changed slope of phase III curve in asthmatic smokers. Short-term use of nicotine-free e-cigarettes increased Raw and decreased sGaw among healthy never smokers. Conclusions Short-term use of an e-cigarette has acute effects on airways physiology and respiratory symptoms in COPD smokers, asthmatic smokers, "healthy" smokers and healthy never smokers. E-cigarette use was associated with effects in "healthy" never smokers irrespectively of nicotine concentration. More studies are needed to investigate both short and long-term effects of e-cigarette use.

Diagnosis of exercise-induced bronchoconstriction (EIB) requires the use of bronchial provocation tests (BPTs). We assessed exercise-induced respiratory symptoms (EIRS), EIB and asthma in athletes and evaluated the validity of BPTs in the diagnosis of EIB. Rhinitis and atopy were also assessed.\ud \ud Athletes with (n = 55) and without previous asthma diagnosis (n = 145) were tested by skin prick tests, lung function and eNO measurements. EIRS were recorded and EIB was assessed by methacholine (Mch), eucapnic voluntary hyperpnoea (EVH), mannitol and exercise test.\ud \ud EIRS were highly reported and history of asthma was common among athletes. A high prevalence of atopy (48.7%) and allergic rhinitis (30.5%) was found. Athletes with asthma had a higher response rate to Mch and to EVH, as compared with athletes without a previous asthma diagnosis (P = 0.012 and P = 0.017 respectively). Report of EIRS, rhinitis and atopy were not associated with a positive BPT response.\ud \ud Screening athletes for EIB using BPTs is suggested, irrespective of reported EIRS or a previous asthma diagnosis.

Interleukin (IL)-18 is a pro-inflammatory cytokine that was firstly described as an interferon (IFN)-γ-inducing factor. Similar to IL-1β, IL-18 is synthesized as an inactive precursor requiring processing by caspase-1 into an active cytokine. The platform for activating caspase-1 is known as the inflammasome, a multiple protein complex. Macrophages and dendritic cells are the primary sources for the release of active IL-18, whereas the inactive precursor remains in the intracellular compartment of mesenchymal cells. Finally, the IL-18 precursor is released from dying cells and processed extracellularly. IL-18 has crucial host defense and antitumor activities, and gene therapy to increase IL-18 levels in tissues protects experimental animals from infection and tumor growth and metastasis. Moreover, multiple studies in experimental animal models have shown that IL-18 over-expression results to emphysematous lesions in mice. The published data prompt to the hypothesis that IL-18 induces a broad spectrum of COPD-like inflammatory and remodeling responses in the murine lung and also induces a mixed type 1, type 2, and type 17 cytokine responses. The majority of studies identify IL-18 as a potential target for future COPD therapeutics to limit both the destructive and remodeling processes occurring in COPD lungs.