Over the past number of decades there has been considerable interest in the role of
neurogenic inflammation in
asthma with the identification of many biologically active
neuropeptides in the lung. Whilst there is convincing evidence of
neurogenic inflammation in various animal models of
asthma, the evidence in humans is less clear and replicating the experimental approaches in humans has proven difficult with different studies producing conflicting results. In terms of human studies, research has focused on whether pro-inflammatory
neuropeptides are elevated in the asthmatic airway, and if so, what their functional effects are. There have also been studies to assess the efficacy of
tachykinin receptor antagonists in improving indices of
asthma control. Information to date would suggest that
neuropeptides are present in human airways and are possibly upregulated in
asthma, but this effect does not appear to be specific and may occur in other inflammatory airways conditions (
chronic obstructive pulmonary disease (
COPD) and smoking). At present there is insufficient evidence to suggest that
tachykinin receptor antagonists confer any additional benefit over inhaled
corticosteroid regimes for asthmatic patients.