TNF and IL‐1β exposure increases airway narrowing but does not alter the bronchodilatory response to deep inspiration in airway segments

Abstract

The failure of DI to produce bronchodilation in patients with asthma may not necessarily involve a direct effect of pro-inflammatory cytokines on airway tissue. A relationship between inflammation and airway hyper-responsiveness is supported, however, regulated by separate disease processes than those which attenuate or abolish the bronchodilatory response to DI in patients with asthma.