Objective To study the role and clinical significance of Toll like receptor 2,4/MyD88/NFκB signaling pathway and related molecules in the pathogenesis of COPD. Methods 112 COPD outpatients were treated with respiratory medicine in our hospital from January 2017 to December 2018, and were divided into observation group (52 cases) and control group (60 cases) according to the progress of the disease. The patients with physical examination in our hospital were selected for the control group (68cases) at the same time. The expression levels of TLR2, TLR4, MyD88 and NFκB mRNA in PBMC of three groups were detected by realtime fluorescent quantitative PCR, and the expressionlevels of IL-1 β, IL-10, TNFα, CRP and sICAM1 in serum of three groups were detected by ELISA. The peripheral blood of patients with AECOPD was cultured with normal saline, LPS, LPS+TLR4Ab, PNG, PNG+TLR2Ab, respectively. The expression of mRNA in PBMC and serum inflammatory factors was detected. Results The levels of TLR2, TLR4, MyD88, NF-B mRNA, and serum IL-1β, IL-10, TNFα, CRP, and sICAM1 in patients with acute exacerbation were significantly higher than those in stable and control group (P＜0.05). The levels of mRNA and serum inflammatory factors in the stable group were higher than those in the control group (P＜0.05). The levels of mRNA and serum inflammatory factors in NS control group were significantly lower than those in other 4 groups(P＜0.05). After LPS treatment alone, all mRNA levels and serum inflammatory factors increased significantly (P＜0.05). After LPS+TLR4Ab treatment, each mRNA level and serum inflammatory factors were significantly reduced (P＜0.05); After PNG treatment alone, all mRNA levels and serum inflammatory factors were significantly increased (P＜0.05). After treatment with PNG+TLR2Ab, all mRNA levels and serum inflammatory factors were significantly reduced(P＜0.05).Conclusion The activation of Tolllike receptor 2,4/ MyD88/ NFB signal pathway in peripheral blood of patients with COPD can increase the release of the downstream inflammatory factors and participate in the inflammatory process of COPD. 