The human microbiome can be defined as the microorganisms that reside within and on our bodies and how they interact with the environment. Recent research suggests that numerous mutually beneficial interactions occur between a human and their microbiome, including those that are essential for good health. Modern microbiological detection techniques have contributed to new knowledge about microorganisms in their human environment. These findings reveal that the microbiomes of the lung and gut contribute to the pathogenesis of asthma and allergy. For example, evidence indicates that the microbiome of the gut regulates the activities of helper T cell subsets (Th1 and Th2) that affect the development of immune tolerance. Moreover, recent studies demonstrate differences between the lung microbiomes of healthy and asthmatic subjects. The hygiene and biodiversity hypotheses explain how exposure to microorganisms is associated with asthma and allergy. Although those living in developed countries are exposed to fewer and less diverse microorganisms compared with the inhabitants of developing countries, they are experiencing an increase in the incidence of asthma and allergies. Detailed analyses of the human microbiome, as are being conducted under the auspices of the Human Microbiome Project initiated in 2007, promise to contribute insights into the mechanisms and factors that cause asthma and allergy that may lead to the development of strategies to prevent and treat these diseases.

Recurrent early life wheeze is not always asthma, and up to 50% of children are reported to remit. With reports of adult asthma symptom relapse, we assessed the prognosis of recurrent bronchial obstruction (rBO) through adolescence in the Environment and Childhood Asthma (ECA) prospective birth cohort study.The present study is based on data from investigations at ages 2, 10 and 16 years of 550 young people (52% males) attending at 16 years of age. Based on the presence of rBO from 0–2 years, defined as recurrent (at least two episodes) doctor-diagnosed wheeze, and asthma from 2–10 years and 10–16 years, defined as at least two episodes of doctor-diagnosed asthma, symptoms and medication use, prognosis of rBO was assessed. Bronchial hyperresponsiveness (BHR) was diagnosed by a metacholine provocation dose ≤8 μmol that caused 20% reduction in the forced expiratory volume in 1 s.At 10–16 years, 34% of the 143 rBO children had asthma. All children with rBO had reduced lung function compared with the never asthmatics. Of the rBO children in remission, 48.4% had asthma symptoms, medication use and/or BHR compared with 26.7% with never asthma (p<0.001).Only 34.3% of rBO children were without asthma symptoms, medication use or BHR by 16 years, possibly indicating future asthma risk.

Rationale: Bronchial hyperresponsiveness (BHR) is an important, but not specific, asthma characteristic. Objectives: We aimed to assess the predictive value of BHR tested by methacholine and exercise challenge at age 10 years for active asthma 6 years later. Methods: From a Norwegian birth cohort, 530 children underwent methacholine challenge and exercise-induced bronchoconstriction (EIB) test (n = 478) at 10 years and structured interview and clinical examination at age 16 years. The methacholine dose causing 20% reduction in FEV1 (PD20) and the reduction in FEV1 (%) after a standardized treadmill test were used for BHR assessment. Active asthma was defined with at least two criteria positive: doctor’s diagnosis of asthma, symptoms of asthma, and/or treatment for asthma in the last year. Measurements and Main Results: PD20 and EIB at 10 years of age increased the risk of asthma (β = 0.94 [95% confidence interval (CI), 0.92–0.96] per μmol methacholine and β = 1.10 [95% CI, 1.06–1.15] per %, respectively). Separately the tests explained 10 and 7%, respectively, and together 14% of the variation in active asthma 6 years later. The predicted probability for active asthma at the age of 16 years increased with decreasing PD20 and increasing EIB. The area under the curve (receiver operating characteristic curves) was larger for PD20 (0.69; 95% CI, 0.62–0.75) than for EIB (0.60; 95% CI, 0.53–0.67). Conclusions: BHR at 10 years was a significant but modest predictor of active asthma 6 years later, with methacholine challenge being superior to exercise test.

Objectives We aimed to examine the effect of β2-agonists on anaerobic performance in healthy non-asthmatic subjects. Design Systematic review and meta-analysis. Eligibility criteria We searched four databases (PubMed, Embase, SPORTDiscus and Web of Science) for randomised controlled trials, published until December 2019, examining the effect of β2-agonists on maximal physical performance lasting 1 min or shorter. Data are presented as standardised difference in mean (SDM) with 95% confidence intervals (95% CI). Results 34 studies were included in the present meta-analysis. The studies include 44 different randomised and placebo-controlled comparisons with β2-agonists comprising 323 participants in crossover trials, and 149 participants in parallel trials. In the overall analyses, β2-agonists improved anaerobic performance by 5% (SDM 0.29, 95% CI 0.16 to 0.42), but the effect was related to dose and administration route. In a stratified analysis, the SDM was 0.14 (95% CI 0.00 to 0.28) for approved β2-agonists and 0.46 (95% CI 0.24 to 0.68) for prohibited β2-agonists, respectively. Furthermore, SDM was 0.16 (95% CI 0.02 to 0.30) for inhaled administration and 0.51 (95% CI 0.25 to 0.77) for oral administration, respectively, and 0.20 (95% CI 0.07 to 0.33) for acute treatment and 0.50 (95% CI 0.20 to 0.80) for treatment for multiple weeks. Analyses stratified for the type of performance showed that strength (0.35, 95% CI 0.15 to 0.55) and sprint (0.17, 95% CI 0.06 to 0.29) performance were improved by β2-agonists. Conclusion/implication Our study shows that non-asthmatic subjects can improve sprint and strength performance by using β2-agonists. It is uncertain, however, whether World Anti-Doping Agency (WADA)-approved doses of β2-agonists improve performance. Our results support that the use of β2-agonists should be controlled and restricted to athletes with documented asthma. Systematic review registration PROSPERO CRD42018109223.