The aim of this study is to investigate the underlying molecular mechanisms that the lncRNA TUG1/miR-145-5p/NF-κB pathway mediates in the hypersusceptibility of airway inflammatory response induced by H3N2 in COPD, thus exploring the underlying mechanisms why AECOPD patients induced by IAV have more severe symptoms and the possible therapeutic strategy. Here, NFKB1 is linked to chronic obstructive pulmonary disease.