• asthma;
  • BDNF;
  • inflammation;
  • lung function;
  • mediator;
  • stress;
  • TNF-α


Background Asthma is a chronic disease defined by airway inflammation, increased airway hyperresponsiveness and episodes of airway obstruction. Although there are abundant clinical and experimental data showing that stress may worsen asthma, the mechanisms linking stress to asthma are not well understood. By inducing a pro-inflammatory cytokine milieu, stress might enhance airway inflammation in bronchial asthma. We therefore investigated the correlation of stress perception and the cytokine profile of circulating lymphocytes in humans.

Methods Allergic asthmatic patients and healthy controls were evaluated for perceived level of stress, demographic and lung function data. Whole blood cells were obtained and stimulated by mitogen to assess intracellular IL-4, IFN-γ and TNF-α by flow cytometry. Neurotrophins nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) were measured in serum.

Results Asthmatic patients showed significantly higher percentages of TNF-α-producing T cells than healthy controls. Only in asthmatic patients was stress perception correlated with percentages of TNF-α-producing T cells and serum BDNF levels, while forced expiratory volume in 1 s (% predicted) was negatively correlated to BDNF.

Conclusion The results of our study support the hypothesis that stress deteriorates bronchial asthma by inducing a pro-inflammatory cytokine profile in allergic asthmatics. Stress management might provide a supplement therapy of allergic asthma.