Abstract
PURPOSE: Emerging evidence suggests that the gut microbiota could be a therapeutic target for asthma via the common mucosal system. The aim of the current study was to investigate the effects of prebiotic Bimuno-galactooligosaccharide (B-GOS) supplementation on hyperpnea-induced bronchoconstriction (HIB), a surrogate for exercise-induced bronchoconstriction (EIB), and airway inflammation in adults with asthma. METHODS: In a double blind cross over trial, 10 participants with asthma and HIB (27 ± 7 years; height: 173 ± 8 cm; body mass: 70 ± 9 kg), and 8 control participants without asthma (age: 26 ± 4 years; height: 174 ± 10 cm; body mass: 72 ± 12 kg) were randomized to receive 5.5 gd-1 of either prebiotic B-GOS or placebo (maltodextrin) for 3 weeks separated by a 2 week washout. HIB severity was based on the peak fall in forced expiratory volume in 1 s (FEV1) following a eucapnic voluntary hyperpnea (EVH) challenge. Markers of airway inflammation included serum concentrations of chemokines (CCL11 and CCL17), tumor necrosis factor alpha (TNF-α), c-reactive protein (CRP), and immunoglobulin E (IgE), and fraction of exhaled nitric oxide (FENO). RESULTS: In the HIB group, the peak fall in FEV1 after EVH was unchanged following placebo (day 0; -880 ± 480 mL, vs day 21; -840 ± 430 mL). Following B-GOS the peak fall in FEV1 after EVH was attenuated by 40% (day 0; -940 ± 460 mL, vs. day 21; -570 ± 310 mL, P = 0.004). No changes in pulmonary function in the control group were evident. In the HIB group B-GOS resulted in baseline reductions in CCL17 (day 0; 399.3 ± 139.6 pg·mL-1, vs. day 21 323.0 ± 133.9 pg·mL-1, P = 0.005) and TNF-α (day 0; 2.68 ± 0.98 pg·mL-1, vs. day 21 2.18 ± 0.59 pg·mL-1, P = 0.004) and the TNF-α increase after EVH was abolished. Baseline CRP was reduced following B-GOS in both the HIB and control groups (P < 0.05). No changes in FENO and CCL11 were evident following either intervention. CONCLUSIONS: B-GOS supplementation attenuated HIB severity in adults with asthma. The associated reduction in markers of airway inflammation suggests that B-GOS may target the underlying immunopathologic features of asthma, thereby attenuating the airway hyperresponsiveness associated with HIB/EIB.
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