Impaired airway epithelial cells can release damage-associated molecular patterns into the extracellular matrix, which target pattern recognition receptors and activate transcription factors such as nuclear factor-κB (NF-κB), to promote the release of various inflammatory substances including TNF-α, IL-6, and IL-1β, and eventually cause airway remodeling, mucus secretion, and emphysema-like injury [6, 35]. This evidence concerns the gene IL1B and pulmonary emphysema.