A 46‐year‐old healthy man developed respiratory distress, night sweats, fever, and weight loss after using electronic cigarettes (e‐cigs) for approximately 1 month. He presented to the hospital when the symptoms worsened 2 months after onset. The findings of bronchoalveolar lavage (BAL) fluid examination and the following transbronchial lung biopsy examination led to the diagnosis of acute alveolitis: intra‐alveolar fibrosis accompanied with exudate containing abundant lipid‐laden macrophages, eosinophils, and neutrophils. Eventually, e‐cig–induced acute lung injury was diagnosed. The symptoms were rapidly alleviated upon e‐cig use termination and methylprednisolone pulse therapy, and no subsequent recurrence was observed. There have been only a few reported cases of e‐cig–induced lung injury. In e‐cig users presenting with atypical pneumonia, close examination by BAL and biopsy should be performed to verify the presence or absence of lipid‐laden macrophages.

This study shows that subjects with long-term outgrown asthma continue to have airway eosinophilic inflammation, airway hyperresponsiveness and airway narrowing.

Background: It has been reported that nasal allergy influences the lower airway inflammation and functions. We elucidated whether nasal allergy would contribute to lower airway inflammation and functions. Methods: 266 subjects aged 21–39 years were interviewed with special emphasis on history of asthma and nasal allergies (perennial allergic rhinitis (PAR) and seasonal allergic rhinitis (Japanese cedar pollinosis; PO)). Symptomatic subject was defined when nasal symptoms were present during a 3-week study period. Pulmonary function, provocative concentration of methacholine causing a 20% fall in forced expiratory volume in 1 s (PC₂₀), capsaicin cough threshold defined as capsaicin concentration eliciting 5 or more coughs (C5) and eosinophil percentage in hypertonic saline-induced sputum were measured. Results: Based on the interview, 232 subjects without asthma were divided into symptomatic (n = 25) and asymptomatic (n = 22) PAR, PO on-season (n = 15) and off-season (n = 36), and non-nasal allergy subjects (control) (n = 134). Sputum eosinophils were significantly greater in symptomatic PAR than another four groups (p < 0.01). FEV₁/FVC ratio was significantly lower in PAR than control (p < 0.05). Maximum mean expiratory flow was lower in PAR than control (asymptomatic: p < 0.05, symptomatic: p = 0.06). C5 was not different among groups. PAR tended to have a lower PC₂₀ compared to control (symptomatic: p = 0.078; asymptomatic: p = 0.086). Conclusions: These results suggest that eosinophilic inflammation occurred in symptomatic period of PAR may contribute to development of lower airway remodeling and bronchial hyperresponsiveness. Reversely, PO may not be associated with lower airway eosinophilic inflammation or abnormal bronchial functions. Nasal allergy dose not influence the cough reflex sensitivity.

Background: Late asthmatic response is observed following antigen challenge in actively, but not passively, sensitized guinea pigs. Although cough reflex sensitivity is increased after antigen challenge in actively sensitized guinea pigs, it is unknown whether the antigen-induced increase in cough reflex sensitivity develops in passively sensitized animals. The aim of this study was to compare the cough reflex sensitivity to inhaled capsaicin after an inhaled antigen challenge between actively and passively sensitized guinea pigs.

Objective A T-SPOT.TB can yield indeterminate results under two test observation conditions: a high response to the nil in negative control wells (high nil-control) or a low response to the mitogen in positive control wells (low mitogen-control). The most strongly influential factors for these indeterminate results, however, have yet to be identified.