Recent investigations suggest that airway wall remodelling and chronic airflow obstruction are almost always associated with increased pulmonary neuroendocrine (NE) cells and increased levels of bombesin-like peptides (BLPs), particularly among cigarette smokers. In contrast, most normal subjects and even smokers who do not develop airflow obstruction do not exhibit such airway wall remodelling, increased NE cells, or increased BLP levels. The hypothesis forwarded, therefore, is that NE cells and BLPs may play a role in the pathogenesis of airway wall remodelling and chronic airflow obstruction.