In COPD, ligands for TLR2 can be PAMPs (lipopeptides, glycolipids, lipoteichoic acid (LTA), peptidoglycan (PGN), etc.)of bacteria colonizing the lower airways (Streptococcus pneumoniae, nontypeable Haemophilus influenzae (NTHi), Moraxella catarrhalis, and Pseudomonas aeruginosa) [44], as well as DAMPs releasing as a result of lung tissue exposure to negative environmental factors, such as smoking [29] and air pollution (high-mobility group protein B1 (HMGPB1), heat shock proteins (HSP60, HSP70), β-defensin, etc.)[45]. This evidence concerns the gene TLR2 and chronic obstructive pulmonary disease.